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1

Elevation of serum soluble intercellular adhesion molecule-1 (sICAM-1) and sE-selectin levels in bronchial asthma.  

PubMed Central

Adhesion molecules such as ICAM-1 and E-selectin have been shown to play important roles in the production of allergic inflammation. In the present study, we measured serum soluble ICAM-1 (sICAM-1) and soluble E-selectin (sE-selectin) levels by ELISA in 42 patients with bronchial asthma (22 atopic and 20 non-atopic) during asthma attacks and in stable conditions in order to assess the state of ICAM-1 and E-selectin in allergic inflammation. Both serum sICAM-1 levels and serum sE-selectin levels in sera obtained during bronchial asthma attacks were higher than those in sera obtained in stable conditions. These findings were observed regardless of atopic status. To examine the regulatory mechanism in the elevation of serum sICAM-1 and sE-selectin levels, serum tumour necrosis factor-alpha (TNF-alpha) levels were measured by ELISA. TNF-alpha levels in sera obtained during bronchial asthma attacks were higher than those in sera obtained in stable conditions. There was a correlation between the nature of change in serum TNF-alpha levels and the nature of change in serum sICAM-1 levels or serum sE-selectin levels, though serum TNF-alpha levels did not correlate with serum sICAM-1 levels or serum sE-selectin levels. These results suggest that higher levels of sICAM-1 and sE-selectin during asthma attacks may reflect the up-regulation of ICAM-1 and E-selectin expression in allergic inflammation, and that the soluble form of these adhesion molecules may be useful markers for the presence of allergic inflammation. TNF-alpha is shown to enhance the expression and release of ICAM-1 and E-selectin in vitro, however; the regulatory mechanism in the elevation of serum sICAM-1 and sE-selectin levels remains to be clarified.

Kobayashi, T; Hashimoto, S; Imai, K; Amemiya, E; Yamaguchi, M; Yachi, A; Horie, T

1994-01-01

2

The probiotic Lactobacillus gasseri SBT2055 inhibits enlargement of visceral adipocytes and upregulation of serum soluble adhesion molecule (sICAM-1) in rats  

Microsoft Academic Search

The probiotic Lactobacillus gasseri strain SBT2055 (LG2055) was tested for its anti-obesity and anti-inflammatory effects to determine health benefits of consuming this organism and to explore possible relationships between those effects. Visceral adipocyte size was used as a measure of obesity, and the level of soluble intercellular adhesion molecule-1 (sICAM-1) in the blood as an inflammatory marker that is elevated

Yukio Kadooka; Akihiro Ogawa; Ken Ikuyama; Masao Sato

2011-01-01

3

Soluble adhesion molecules (sICAM-1, sVCAM-1) and selectins (sE selectin, sP selectin, sL selectin) levels in children and adolescents with obesity, hypertension, and diabetes  

Microsoft Academic Search

The attachment of monocytes and lymphocytes to endothelial cells, which initiates atherosclerosis, arises under the influence of adhesion molecules. The preclinical phase of this disease lasts many decades, and this provides an opportunity for the presymptomatic detection of high-risk subjects. We evaluated levels of the adhesion molecules: sICAM-1 (soluble intercellular adhesion molecule 1), sVCAM-1 (soluble vascular adhesion molecule 1), sE

Barbara Glowinska; Miroslawa Urban; Jadwiga Peczynska; Bozena Florys

2005-01-01

4

Circulating selectins, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 in hyperthyroidism.  

PubMed

Serum concentrations of soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble E-selectin (sE-selectin), soluble P-selectin, and soluble L-selectin (sL-selectin), tumor necrosis factor-alpha, and interleukin-6 were measured in patients with Graves' disease (GD) (n = 33), in patients with toxic nodular goiter (n = 34), and in a group of healthy controls (n = 36). The serum levels of sICAM-1, sVCAM-1, sE-selectin, and sL-selectin were markedly elevated in patients with GD and in patients with toxic nodular goiter before treatment with methimazole (P < 0.05 for all). After 8 weeks of therapy, serum concentrations of sVCAM-1 and sE-selectin normalized, whereas serum levels of sL-selectin and sICAM-1 remained elevated. Hormone concentrations normalized after 2 weeks, clearly preceding falling levels of circulating adhesion molecules. Serum concentrations of soluble P-selectin, TNF-alpha, and interleukin-6 did not differ among patients with GD and toxic nodular goiter and healthy subjects. Serum levels of sVCAM-1 and sICAM-1 correlated with the serum concentrations of TSH receptor antibodies (n = 33; r = 0.921 and r = 0.792, respectively) and thyroid peroxidase antibodies (n = 33; r = 0.682 and r = 0.761, respectively) but not thyroglobulin antibodies. However, no correlation between serum levels of sE-selectin, sL-selectin, and soluble P-selectin or cytokines and serum levels of thyroid peroxidase antibodies, TSH receptor antibodies, or thyroglobulin antibodies, respectively, was found. In addition, no correlation between serum levels of adhesion molecules or cytokines and thyroid hormones was seen. We conclude that both the action of thyroid hormones and the autoimmune process in GD may contribute to elevated levels of soluble adhesion molecules. PMID:7541802

Wenisch, C; Myskiw, D; Gessl, A; Graninger, W

1995-07-01

5

Differential up-regulation of circulating soluble and endothelial cell intercellular adhesion molecule-1 in mice.  

PubMed Central

Although circulating levels of soluble intercellular adhesion molecule-1 (sICAM-1) are frequently used as an indicator of the severity of different immune, inflammatory, or neoplastic diseases, little is known about the factors that govern plasma sICAM-1 concentration and its relationship to the membranous form of ICAM-1 (mICAM-1) expressed on vascular endothelial cells. Plasma sICAM-1 concentration (measured by enzyme-linked immunosorbent assay) and mICAM-1 expression (measured using the dual radiolabeled monoclonal antibody technique) in different vascular beds (eg, lung, small intestine, and spleen) were monitored in wild-type (C57BL) and ICAM-1-deficient mice, before and after administration of tumor necrosis factor (TNF)-alpha. In wild-type mice, TNF-alpha elicited time-dependent increases in lung and intestine mICAM-1 (plateau achieved at 12 hours), with a corresponding increase in plasma sICAM-1 (peaked at 5 hours and then declined). The initial increases in mICAM-1 and pulmonary leukocyte sequestration (measured as lung myeloperoxidase activity) induced by TNF-alpha preceded any detectable elevation in sICAM-1. In ICAM-1-deficient mice, plasma sICAM-1 was reduced by approximately 70%, with > 95% reductions of mICAM-1 in lung and intestine, and > 75% reduction in splenic accumulation of anti-ICAM-1 antibody. Although TNF-alpha doubled plasma sICAM-1 in ICAM-1-deficient mice, mICAM-1 was unaffected in all tissues. Either splenectomy or pretreatment with cycloheximide resulted in an attenuated TNF-induced increase in sICAM-1, without affecting mICAM-1 expression. These findings indicate that plasma sICAM-1 concentration does not accurately reflect the level of ICAM-1 expression on endothelial cells in different vascular beds.

Komatsu, S.; Flores, S.; Gerritsen, M. E.; Anderson, D. C.; Granger, D. N.

1997-01-01

6

Increased levels of serum intercellular adhesion molecule 1 in HIV infection are related to immune activation.  

PubMed

Cytopathic mechanisms in human immunodeficiency virus type 1 (HIV-1) infection involve syncytia formation, and it appears likely that increased expression of intracellular adhesion molecule 1 (ICAM-1) is involved in these cell adhesion phenomena. In this study, we determined serum concentrations of soluble ICAM-1 (sICAM-1) in 27 patients with HIV-1 infection and a control group. In addition, we compared sICAM-1 values to CD4+ T-cell counts, serum beta 2-microglobulin (beta 2M) and serum neopterin levels. HIV-1-infected patients had significantly higher sICAM-1, beta 2M and neopterin levels than controls. The subgroup of patients with Walter-Reed stages 3-6 had only slightly higher sICAM-1 concentrations in serum than Walter-Reed stages 1-2. The sICAM-1 concentrations in HIV-1-seropositive patients correlated with beta 2M levels but neither with neopterin nor with CD4+ T-cell counts. Increased sICAM-1 may result from immune activation, which enhances the expression of ICAM-1 in patients with HIV-1 infection. PMID:8104576

Diez-Ruiz, A; Kaiser, G; Jäger, H; Birkmann, J; Tilz, G P; Wachter, H; Fuchs, D

1993-01-01

7

The Role of Intercellular Adhesion Molecule1 (ICAM-1), Vascular Cell Adhesion Molecule1 (VCAM-1), and Regulated on Activation, Normal T-Cell Expressed and Secreted (RANTES) in the Relationship between Air Pollution and Asthma among Children  

Microsoft Academic Search

To evaluate the role of adhesion molecules and chemokines in the relationship between air pollution and asthma, the authors determined the following in 230 children who lived in 4 communities in Japan that had different levels of air pollution: serum concentrations of soluble intercellular adhesion molecule-1 (sICAM-1); soluble vascular cell adhesion molecule-1 (sVCAM-1); regulated on activation, normal T-cell expressed and

Michiko Ando; Masayuki Shima; Motoaki Adachi; Yoshizo Tsunetoshi

2001-01-01

8

Intraocular soluble intracellular adhesion molecule-1 correlates with subretinal fluid height of diabetic macular edema  

PubMed Central

Objective: To investigate the correlations between aqueous concentrations of vascular endothelial growth factor (VEGF), monocyte chemoattractant protein-1 (MCP-1), soluble intracellular adhesion molecule-1 (sICAM-1) and diabetic macular edema (DME). Materials and Methods: VEGF, MCP-1 and sICAM-1 concentrations in aqueous humor samples of 22 patients with DME and 23 patients with cataract of a control group were measured with solid-phase chemiluminescence immunoassay. Results: Aqueous VEGF (89.2 ± 58.5 pg/ml versus 48.5 ± 27.8 pg/ml, P = 0.006), MCP-1 (684.2 ± 423.4 pg/ml versus 432.4 ± 230.4 pg/ml, P = 0.019) and sICAM-1 (3213.8 ± 2581.6 pg/ml versus 260.2 ± 212.2 pg/ml, P < 0.001) all vary significantly between DME group and control group. Maximum height of submacular fluid measured by Optical coherence tomography (OCT) was significantly associated with aqueous sICAM-1 (r = -0.45, P = 0.034). The maximum height of macular thickness measured by OCT was not significantly associated with either VEGF (P = 0.300), MCP-1 (P = 0.320) or sICAM-1 (P = 0.285). Conclusions: Our results suggest that sICAM-1 may majorly contribute to the formation of subretinal fluid in DME patients and imply that MCP-1 and sICAM-1 may be the potential therapy targets, besides VEGF.

Zhu, Dan; Zhu, He; Wang, Chunyan; Yang, Dayong

2014-01-01

9

Prognostic value of serum CD44, intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 levels in patients with indolent non-Hodgkin lymphomas.  

PubMed

Elevated serum CD44, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) have been linked to poor prognosis in aggressive lymphomas, but their utility in low grade lymphomas remains undefined. We evaluated serum CD44, VCAM-1 and ICAM-1 levels in 100 patients with newly diagnosed indolent NHL. The median pre-treatment values of the markers were as follows: CD44 540 ng/mL (range 156-1201), ICAM-1 311 ng/mL (range 102-1222) and VCAM-1 1165 ng/mL (range 248-4779). On univariate analysis, elevated sCD44, sICAM-1 and sVCAM-1 were significantly associated with worse overall (OS) and progression-free survival (PFS). In a subset analysis of patients with stage IV disease, the effects of sCD44 and sICAM-1 on OS persisted (p<0.05), as did the effect of sCD44 on PFS (p<0.01). In a multivariate analysis that included conventional prognostic factors and the Follicular Lymphoma International Prognostic Index (FLIPI) model, sICAM-1 demonstrated prognostic value for OS and PFS. We conclude that serum CD44, ICAM-1 and VCAM-1 can potentially be prognostic in patients with indolent NHL. Though the FLIPI model remains the gold standard for prognosis, these quantitative serologic markers may be useful as adjunct tools in assessing disease risk. PMID:21895545

Shah, Nina; Cabanillas, Fernando; McIntyre, Bradley; Feng, Lei; McLaughlin, Peter; Rodriguez, Maria A; Romaguera, Jorge; Younes, Anas; Hagemeister, Fredrick B; Kwak, Larry; Fayad, Luis

2012-01-01

10

Disturbed Homeostasis of Lung Intercellular Adhesion Molecule-1 and Vascular Cell Adhesion Molecule-1 During Sepsis  

PubMed Central

Cecal ligation and puncture (CLP)-induced sepsis in mice was associated with perturbations in vascular adhesion molecules. In CLP mice, lung vascular binding of 125I-monoclonal antibodies to intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 revealed sharp increases in binding of anti-ICAM-1 and significantly reduced binding of anti-VCAM-1. In whole lung homogenates, intense ICAM-1 up-regulation was found (both in mRNA and in protein levels) during sepsis, whereas very little increase in VCAM-1 could be measured although some increased mRNA was found. During CLP soluble VCAM-1 (sVCAM-1) and soluble ICAM-1 (sICAM-1) appeared in the serum. When mouse dermal microvascular endothelial cells (MDMECs) were incubated with serum from CLP mice, constitutive endothelial VCAM-1 fell in association with the appearance of sVCAM-1 in the supernatant fluids. Under the same conditions, ICAM-1 cell content increased in MDMECs. When MDMECs were evaluated for leukocyte adhesion, exposure to CLP serum caused increased adhesion of neutrophils and decreased adhesion of macrophages and T cells. The progressive build-up in lung myeloperoxidase after CLP was ICAM-1-dependent and independent of VLA-4 and VCAM-1. These data suggest that sepsis disturbs endothelial homeostasis, greatly favoring neutrophil adhesion in the lung microvasculature, thereby putting the lung at increased risk of injury.

Laudes, Ines J.; Guo, Ren-Feng; Riedemann, Niels C.; Speyer, Cecilia; Craig, Ron; Sarma, J. Vidya; Ward, Peter A.

2004-01-01

11

Serum levels of soluble platelet endothelial cell adhesion molecule-1 and vascular cell adhesion molecule-1 are decreased in subjects with autism spectrum disorder  

PubMed Central

Background Adhesion molecules, such as platelet-endothelial adhesion molecule-1 (PECAM-1), platelet selectin (P-selectin), endothelial selectin (E-selectin), intracellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1), are localized on the membranes of activated platelets and leukocytes and on the vascular endothelium. Recently, we measured serum levels of soluble (s) forms of adhesion molecules in adults,18 to 26 years old, with autism spectrum disorder (ASD) and observed low levels of sPECAM-1 and sP-selectin. A subsequent study showed a similar result in children two to four years old with ASD. However, information about school age (five to seventeen years old) ASD subjects is required to determine whether adhesion molecules are also reduced in individuals with ASD in this age range. Findings Twenty-two subjects with high-functioning ASD and 29 healthy age-matched controls were recruited. ELISA was used for sPECAM-1, and a suspension array system was used for sP-selectin, sE-selectin, sICAM-1 and sVCAM-1 measurements. We found that serum levels of sPECAM-1 (U = 91.0, P<0.0001 by Mann–Whitney U test) and sVCAM-1 (U = 168.0, P = 0.0042) were significantly lower in ASD subjects than in controls. Subsequently, we examined the correlations between serum levels of either sPECAM-1 or sVCAM-1 and clinical variables including Autism Diagnostic Interview - Revised subscores and our previous cytokine profile data from the same ASD subjects. However, we did not find any significant correlations between them. Conclusions The present results, taken together with previous results, suggest that sPECAM-1 may play a role in the generation and development of ASD, beginning in childhood and lasting until adulthood.

2013-01-01

12

Evaluation of serum levels of cytokines and intercellular adhesion molecule-1 (ICAM-1) in astrocytic tumours.  

PubMed

Soluble form of intercellular adhesion molecules (sICAM) are increased in serum of many inflammatory diseases and tumours: the expression of such molecules is regulated by cytokines. In the present paper serum levels of interleukin-2 (IL-2), soluble interleukin-2 receptor (sIL-2R) and sICAM-1 were evaluated in patients with glioma compared with different tumours (lung and kidney carcinoma) in order to investigate the compromise of the immune system in these malignancies and to understand the host defence mechanisms. 14 cases of astrocytomas (WHO grade II, III), 20 cases of glioblastomas (GBL, WHO grade IV), 5 cases of lung carcinoma and 6 cases of kidney carcinoma were studied; the results were compared with 15 healthy controls. IL-2, sIL-2R, sICAM-1 concentrations were assessed by an enzyme-linked immunosorbent assay (ELISA) technique. The results were analyzed by Student's t test. Our findings showed that serum levels of IL-2 and sIL-2R were increased in all cancer patients; on the contrary, sICAM-1 serum levels were not significantly increased in GBL and astrocytoma patients. The increased values of IL-2 and sIL-2R are in agreement with a depression of the immune reactivity in patients with glioblastoma and astrocytoma, as reported in literature. On the contrary the levels of sICAM-1 are unchanged in astrocytic tumours while patients with kidney carcinoma presented the higher levels and an unfavourable prognosis. PMID:12899444

Nano, R; Capelli, E; Argentina, F; Facoetti, A; Gerzeli, G

2003-06-01

13

Intercellular adhesion molecule-1 (ICAM-1) gene polymorphisms in endometriosis  

Microsoft Academic Search

Endometriosis is a gynaecological disease with a certain genetic background, but the locations of possible genomic aberrations are still poorly clarified. Intercellular adhesion molecule-1 (ICAM-1), which is a surface glycoprotein that promotes adhesion in immunological and inflammatory reactions, seems to play a role in this condition. The aim of this study was to examine the potential associations of ICAM-1 gene

P. Vigano; M. Infantino; D. Lattuada; R. Lauletta; E. Ponti; E. Somigliana; M. Vignali; A. M. DiBlasio

2003-01-01

14

Inverse correlation between coronary blood flow velocity and sICAM-1 level observed in ischemic heart disease patients.  

PubMed

Systemic factors and blood flow velocity related to atherosclerosis have been examined mainly separately or by in vitro studies. The aim of our study was to investigate the association between local coronary blood flow (corrected TIMI frame count, CTFC) and systemic atherosclerosis-related inflammatory parameters such as soluble intercellular adhesion molecule-1 (sICAM-1), interleukin-6 (Il-6), high sensitivity C-reactive protein (hsCRP) and von Willebrand factor (vWF) in humans. We enrolled the following groups of ischemic heart disease (IHD) patients: patients with coronary stenosis and stable (CAD, n = 96) or unstable angina (ACS, n = 27), patients with documented myocardial ischemia and normal coronary angiogram (NEG, n = 68). Patient groups showed only marginal differences in CTFC or sICAM-1 levels. In contrast, when IHD patients were studied individually, general positive correlation was found between CTFC and sICAM-1 level (r = 0.33; in NEG r = 0.25; in CAD r = 0.37; in ACS r = 0.61), being the strongest in ACS. The relation was independent from age, gender, BMI, smoking, hypertension, diabetes, previous myocardial infarction, family history of IHD, medication, hsCRP, IL-6 and vWF levels. (odds ratio, OR = 6.4; CI 95%: 2.43-16.84; p < 0.05). Nevertheless, correlation between CTFC and IL-6, hsCRP, vWF levels was not found. These results indicate inverse correlation between coronary blood flow and adhesion molecule production independently from conventional cardiovascular risk factors and inflammatory markers. PMID:16297392

Bencze, Jusztina; Kiss, Robert Gabor; Toth-Zsamboki, Emese; Vargova, Katarina; Kerecsen, Gabor; Korda, Andras; Molnar, Ferenc; Preda, Istvan

2006-09-01

15

E-selectin and intercellular adhesion molecule-1 are released by activated human endothelial cells in vitro.  

PubMed Central

Endothelial cells respond to several cytokines by a rapid increase in expression of the adhesion molecules E-selectin and intercellular adhesion molecule-1 (ICAM-1), followed by a gradual decline. The fate of these molecules, which was so far unknown, was studied. Specific sandwich ELISA for the detection of soluble (s)E-selectin and sICAM-1 were developed. In supernatant, centrifuged 3 hr at 100,000 g to remove microparticles, from human umbilical vein endothelial cells (HUVEC) activated with tumour necrosis factor (TNF), interleukin-1 (IL-1) or lipopolysaccharide (LPS), E-selectin and ICAM-1 molecules could be detected. Biochemical analysis revealed that sE-selectin migrated as a band of approximately 94,000 MW. The amount of soluble adhesion molecules released was directly correlated with cell surface expression. Maximal release of E-selectin was observed 6-12 hr after activation of HUVEC and decreased to below detection limit 24 hr after activation. After activation, release of ICAM-1 gradually increased with ICAM-1 cell surface expression, and reached a plateau after 24 hr, which was constant for 3 days. Since E-selectin and ICAM-1 are highly expressed at inflammatory sites, the resulting high concentrations of released E-selectin and ICAM-1 may affect interactions of leucocytes with endothelial cells. The physiological role, however, of the release of E-selectin and ICAM-1 remains to be elucidated. Images Figure 6

Leeuwenberg, J F; Smeets, E F; Neefjes, J J; Shaffer, M A; Cinek, T; Jeunhomme, T M; Ahern, T J; Buurman, W A

1992-01-01

16

Alterations of the CD4(+), CD8 (+) T cell subsets, interleukins-1beta, IL-10, IL-17, tumor necrosis factor-alpha and soluble intercellular adhesion molecule-1 in rheumatoid arthritis and osteoarthritis: preliminary observations.  

PubMed

Rheumatoid arthritis is a multisystem disease with underlying immune mechanisms. Osteoarthritis is a debilitating, progressive disease of diarthrodial joints associated with the aging process. Although much is known about the pathogenesis of rheumatoid arthritis and osteoarthritis, our understanding of some immunologic changes remains incomplete. This study tries to examine the numeric changes in the T cell subsets and the alterations in the levels of some cytokines and adhesion molecules in these lesions. To accomplish this goal, peripheral blood and synovial fluid samples were obtained from 24 patients with rheumatoid arthritis, 15 patients with osteoarthritis and six healthy controls. The counts of CD4 (+) and CD8 (+) T lymphocytes were examined using flow cytometry. The levels of some cytokines (TNF-alpha, IL1-beta, IL-10, and IL-17) and a soluble intercellular adhesion molecule-1 (sICAM-1) were measured in the sera and synovial fluids using enzyme linked immunosorbant assay. We found some variations in the counts of T cell subsets, the levels of cytokines and sICAM-1 adhesion molecule between the healthy controls and the patients with arthritis. High levels of IL-1beta, IL-10, IL-17 and TNF-alpha (in the serum and synovial fluid) were observed in arthritis compared to the healthy controls. In rheumatoid arthritis, a high serum level of sICAM-1 was found compared to its level in the synovial fluid. A high CD4(+)/CD8(+) T cell ratio was found in the blood of the patients with rheumatoid arthritis. In rheumatoid arthritis, the cytokine levels correlated positively with some clinicopathologic features. To conclude, the development of rheumatoid arthritis and osteoarthritis is associated with alteration of the levels of some cytokines. The assessment of these immunologic changes may have potential prognostic roles. PMID:18392953

Hussein, Mahmoud R; Fathi, Nehal A; El-Din, Azza M Ezz; Hassan, Hewayda I; Abdullah, Fatemah; Al-Hakeem, Eman; Backer, Eman Abo

2008-09-01

17

Elevated Circulating E-Selectin, Intercellular Adhesion Molecule 1, and von Willebrand Factor in Patients with Severe Infection  

Microsoft Academic Search

To investigate interactions between the endothelium and leukocytes in patients with sepsis, we mea- sured soluble adhesion molecules (sE-selectin and sICAM-1), von Willebrand factor antigen (vWf:Ag), myeloperoxidase (MPO), and lactoferrin (Lacto- f ) as plasma markers of endothelial and neutrophil activation. We tested whether the five proteins were predictors of clinical severity, which was evalu- ated by simplified acute physiological

SAMER KAYAL; JEAN-PHILIPPE JAÏS; NADIA AGUINI; JEAN CHAUDIÈRE; JACQUES LABROUSSE

1998-01-01

18

Soluble interleukin-2 receptor, soluble CD8 and soluble intercellular adhesion molecule-1 levels in hematologic malignancies.  

PubMed

Plasma levels of soluble interleukin-2 receptor (sIL-2R), soluble CD8 (sCD8) and soluble intercellular adhesion molecule 1 (sICAM-1) were determined by ELISA assays in about 100 patients with hairy cell leukemia (HCL), acute myelomonocytic leukemia (AMMoL), acute myelocytic leukemia (AML), chronic lymphocytic leukemia (CLL), prolymphocytic leukemia (PLL), acute lymphoblastic leukemia (ALL), adult T-cell leukemia (ATL), and mycosis fungoides (MF). Additionally, cultured AML, ALL, and CLL cells grown with and without 12-0-tetra-decanoyl-phorbol-13-acetate (TPA) were tested for IL-2R (CD25) expression by indirect immunofluorescence. Supernatants of these cultures were also tested for sIL-2R by ELISA. Elevated sIL-2R levels were found in HCL patients at initial diagnosis and relapse, in AMMoL, in AML, in the accelerated and non-accelerated phases of B-CLL, in PLL, in non-T/non-B ALL, in B-ALL in mixed lineage ALL, in T-CLL, in T-ALL, and in active MF. Reduced levels of sIL-2R were encountered in HCL patients in remission, in pre-T-ALL, and in MF patients in remission. Also, in non-accelerated CLL sIL-2R levels were less elevated than in later stages of the disease. In T-CLL, sIL-2R was only slightly elevated. Thus, we believe sIL-2R could prove to be a useful marker of disease stage, subtype, and prognosis in several hematologic malignancies. The cultures with and without TPA suggested that the undetermined source of sIL-2R in HCL, ALL and AML could indeed be the malignant cells but perhaps not so in the case of B-CLL. Plasma sCD8 was found to be below normal control levels in HCL, and lowest in relapsing cases. In addition, sCD8 levels were below normal in pre-T-ALL, and in MF. Levels in the non-accelerated phase of B-CLL approximated those of controls. Elevated levels of sCD8 were observed in AML, AMMoL, accelerated stage B-CLL, PLL, non-T/non-B ALL, B-ALL, mixed lineage ALL, T-ALL, T-CLL, and ATL. Thus, in a few instances, sCD8 may also correlate with disease subtype, as well as stage. Although sICAM-1 levels were elevated in all leukemias, its levels in CLL did not appear to be related to disease activity. Whether this is true or not for other leukemias would require additional work on sICAM-1 levels and its relationship to disease activity and prognosis. PMID:7909467

Srivastava, M D; Srivastava, A; Srivastava, B I

1994-01-01

19

Dipeptidyl peptidase-4 inhibition with saxagliptin enhanced nitric oxide release and reduced blood pressure and sICAM-1 levels in hypertensive rats.  

PubMed

Most patients with diabetes also have hypertension, a risk factor associated with atherothrombotic disease and characterized by endothelial cell (EC) dysfunction and loss of nitric oxide (NO) bioavailability. Recent studies suggest a possible antihypertensive effect with dipeptidyl peptidase-4 (DPP4) inhibition; however, the underlying mechanism is not understood. In this study, we tested the effects of the DPP4 inhibitor, saxagliptin, on EC function, blood pressure, and soluble intercellular adhesion molecule 1 (sICAM-1) levels in hypertensive rats. Spontaneously hypertensive rats were treated with vehicle or saxagliptin (10 mg·kg(-1)·day(-1)) for 8 weeks. NO and peroxynitrite (ONOO(-)) release from aortic and glomerular ECs was stimulated with calcium ionophore and measured using electrochemical nanosensor technology. Changes in EC function were correlated with fasting glucose levels. Saxagliptin treatment was observed to increase aortic and glomerular NO release by 22% (P < 0.001) and 23% (P < 0.001), respectively, with comparable reductions in ONOO(-) levels; the NO/ONOO(-) ratio increased by >50% in both EC types (P < 0.001) as compared with vehicle. Saxagliptin also reduced mean arterial pressure from 170 ± 10 to 158 ± 10 mm Hg (P < 0.001) and decreased sICAM-1 levels by 37% (P < 0.01). The results of this study suggest that DPP4 inhibition reduces blood pressure and inflammation in hypertensive rats while increasing NO bioavailability. PMID:22932707

Mason, R Preston; Jacob, Robert F; Kubant, Ruslan; Ciszewski, Aleksander; Corbalan, J Jose; Malinski, Tadeusz

2012-11-01

20

Intercellular Adhesion Molecule1 Dimerization and Its Consequences for Adhesion Mediated by Lymphocyte Function Associated1  

Microsoft Academic Search

Summary Intercellular adhesion molecule-1 (ICAM-1, CD54) is a ligand for the integrins lymphocyte function associated-1 (LFA-1, CD11a\\/CD18) and complement receptor-3 (Mac-l, CD11b\\/ CD 18) making it an important participant in many immune and inflammatory processes. Mod- ified recombinant soluble ICAM-1 formed dimers. This result indicated that the ectodomain of ICAM-1 contains homophilic interaction sites. Soluble ICAM-1 dimers bind to solid-phase

Jim Miller; Ruth Knorr; Marco Ferrone; Roya Houdei; Christopher E Carron; Michael L. Dustin

21

Angiogenesis in platelet endothelial cell adhesion molecule-1-null mice.  

PubMed

Platelet endothelial cell adhesion molecule (PECAM)-1 has been previously implicated in endothelial cell migration; additionally, anti-PECAM-1 antibodies have been shown to inhibit in vivo angiogenesis. Studies were therefore performed with PECAM-1-null mice to further define the involvement of PECAM-1 in blood vessel formation. Vascularization of subcutaneous Matrigel implants as well as tumor angiogenesis were both inhibited in PECAM-1-null mice. Reciprocal bone marrow transplants that involved both wild-type and PECAM-1-deficient mice revealed that the impaired angiogenic response resulted from a loss of endothelial, but not leukocyte, PECAM-1. In vitro wound migration and single-cell motility by PECAM-1-null endothelial cells were also compromised. In addition, filopodia formation, a feature of motile cells, was inhibited in PECAM-1-null endothelial cells as well as in human endothelial cells treated with either anti-PECAM-1 antibody or PECAM-1 siRNA. Furthermore, the expression of PECAM-1 promoted filopodia formation and increased the protein expression levels of Cdc42, a Rho GTPase that is known to promote the formation of filopodia. In the developing retinal vasculature, numerous, long filamentous filopodia, emanating from endothelial cells at the tips of angiogenic sprouts, were observed in wild-type animals, but to a lesser extent in the PECAM-1-null mice. Together, these data further establish the involvement of endothelial PECAM-1 in angiogenesis and suggest that, in vivo, PECAM-1 may stimulate endothelial cell motility by promoting the formation of filopodia. PMID:19574426

Cao, Gaoyuan; Fehrenbach, Melane L; Williams, James T; Finklestein, Jeffrey M; Zhu, Jing-Xu; Delisser, Horace M

2009-08-01

22

The influence of garlic (Allium sativum) extract on interleukin 1alpha-induced expression of endothelial intercellular adhesion molecule-1 and vascular cell adhesion molecule-1.  

PubMed

Inflammation plays an important role in both the initiation of atherosclerosis and development of atherothrombotic events. The adherence of leukocytes/monocytes to the endothelium is an early event in atherogenesis. Phytotherapeutica as garlic and garlic extracts were shown to have beneficial modulating effects in patients with atherosclerotic disease. The aim of this study was to evaluate in vitro the influence of water-soluble garlic (Allium sativum) extract on the cytokine-induced expression of endothelial leukocyte adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1, CD54) and vascular cell adhesion molecule-1 (VCAM-1, CD106). Cytokine-induced expression of cellular adhesion molecules was measured on primary human coronary artery endothelial cell (HCAEC) cultures. HCAEC were cultured in microvascular endothelial cell growth medium and preincubated with garlic extract at various concentrations (0.25-4.0 mg/ml), after which human interleukin-1alpha (IL-1alpha, 10 ng/ml) was added for 1 day. Fluorescein isothiocyanate (FITC)-labeled anti-ICAM-1 and FITC-labeled anti-VCAM-1 were used to analyze the IL-1alpha-induced expression of ICAM-1 and VCAM-1 by flow cytometry. Incubation of HCAEC with garlic extract significantly decreased ICAM-1 and VCAM-1 expression induced by IL-1alpha. In addition, we examined the effects of garlic extract on the adhesion of monocytes to endothelial cells, using the monocytic U937 cell line. The presence of garlic extract significantly inhibited the adhesion of monocytes to IL-1alpha-stimulated endothelial cells. These results indicate that garlic extract modulates the expression of ICAM-1 and VCAM-1, thus potentially contributing to the beneficial effects traditionally attributed to garlic. PMID:16492524

Rassoul, F; Salvetter, J; Reissig, D; Schneider, W; Thiery, J; Richter, V

2006-03-01

23

Inhibitors of 5-lipoxygenase inhibit expression of intercellular adhesion molecule-1 in human melanoma cells1  

Microsoft Academic Search

AIM: To study the effect of 5-lipoxygenase inhibitors on the expression of intercellular adhesion molecule-1 (ICAM-1) in melanoma cells. METHODS: ICAM-1 protein of human melanoma cell a375 was detected by enzyme-linked immunosorbent, flow cytometry and Western blot analysis. Level of ICAM-1 mRNA in a375 was evaluated by Northern blot analysis. Adhesion of a375 to endothelial cell EC304 was analyzed by

Yin WANG; Bin ZHOU; Ji LI; Yong-bing CAO; Xin-sheng CHEN; Ming-he CHENG; Ming YIN

24

Endothelial Leukocyte Adhesion Molecule 1: Direct Expression Cloning and Functional Interactions  

Microsoft Academic Search

A cDNA for endothelial leukocyte adhesion molecule 1 (ELAM-1) was isolated by transient expression in COS-7 cells of a subtracted cDNA library from cytokine-treated human umbilical vein endothelial cells (HUVECs), with selection of ELAM-1-expressing clones by adhesion of transfected cells to the human promyelocytic cell line HL-60. This cloning method requires neither antibody nor purified ligand. ELAM-1-expressing COS cells bind

C. Hession; L. Osborn; D. Goff; G. Chi-Rosso; C. Vassallo; M. Pasek; C. Pittack; R. Tizard; S. Goelz; K. McCarthy; S. Hopple; R. Lobb

1990-01-01

25

Shear stress selectively upregulates intercellular adhesion molecule-1 expression in cultured human vascular endothelial cells.  

PubMed Central

Hemodynamic forces induce various functional changes in vascular endothelium, many of which reflect alterations in gene expression. We have recently identified a cis-acting transcriptional regulatory element, the shear stress response element (SSRE), present in the promoters of several genes, that may represent a common pathway by which biomechanical forces influence gene expression. In this study, we have examined the effect of shear stress on endothelial expression of three adhesion molecules: intercellular adhesion molecule-1 (ICAM-1), which contains the SSRE in its promoter, and E-selectin (ELAM-1) and vascular cell adhesion molecule-1 (VCAM-1), both of which lack the SSRE. Cultured human umbilical vein endothelial cells, subjected to a physiologically relevant range of laminar shear stresses (2.5-46 dyn/cm2) in a cone and plate apparatus for up to 48 h, showed time-dependent but force-independent increases in surface immunoreactive ICAM-1. Upregulated ICAM-1 expression was correlated with increased adhesion of the JY lymphocytic cell line. Northern blot analysis revealed increased ICAM-1 transcript as early as 2 h after the onset of shear stress. In contrast, E-selectin and vascular cell adhesion molecule-1 transcript and cell-surface protein were not upregulated at any time point examined. This selective regulation of adhesion molecule expression in vascular endothelium suggests that biomechanical forces, in addition to humoral stimuli, may contribute to differential endothelial gene expression and thus represent pathophysiologically relevant stimuli in inflammation and atherosclerosis. Images

Nagel, T; Resnick, N; Atkinson, W J; Dewey, C F; Gimbrone, M A

1994-01-01

26

Intercellular Adhesion Molecule 1 Mediates Mononuclear Cell Infiltration into Rat Glomeruli after Renal Ablation  

Microsoft Academic Search

Mononuclear cells, primarily macrophages and lymphocytes, infiltrate the renal glomeruli and are involved in the progression of various glomerular diseases. Intercellular adhesion molecule 1 (ICAM-1) is expressed on the vascular endothelium and mediates the infiltration of leukocytes into the site of inflammation. Although the expression of ICAM-1 can be induced by the stimulation of inflammatory cytokine, ICAM-1 expression can also

Nobuyuki Miyatake; Kenichi Shikata; Hikaru Sugimoto; Masahiko Kushiro; Yasushi Shikata; Saeko Ogawa; Yoshiko Hayashi; Masayuki Miyasaka; Hirofumi Makino

1998-01-01

27

Elevated Serum Vascular Cell Adhesion Molecule-1 Is Associated with Septic Encephalopathy in Adult Community-Onset Severe Sepsis Patients  

PubMed Central

Background and Aim. Septic encephalopathy (SE) is a common complication of severe sepsis. Increased concentrations of circulating soluble adhesion molecules are reported in septic patients. This study aimed to determine whether serum adhesion molecules are associated with SE. Methods. Seventy nontraumatic, nonsurgical adult patients with severe sepsis admitted through ER were evaluated. Serum adhesion molecules were assessed for their relationship with SE, and compared with other clinical predictors and biomarkers. Results. Twenty-three (32.8%) patients had SE. SE group had higher in-hospital mortality (40% versus 11%, P = 0.009) and their sVCAM-1, sICAM-1, and lactate levels on admission were also higher than non-SE group. By stepwise logistic regression model, sVCAM-1, age, and maximum 24-hours SOFA score were independently associated with septic encephalopathy. The AUC analysis of ROC curve of different biomarkers showed that sVCAM-1 is better to predict SE. The sVCAM-1 levels in the SE group were significantly higher than those of the non-SE group at three time periods (Days 1, 4, and 7). Conclusions. Septic encephalopathy implies higher mortality in nontraumatic, nonsurgical patients with severe sepsis. VCAM-1 level on presentation is a more powerful predictor of SE in these patients than lactate concentration and other adhesion molecules on admission.

Su, Chih-Min; Cheng, Hsien-Hung; Tsai, Tsung-Cheng; Hsiao, Sheng-Yuan; Tsai, Nai-Wen; Chang, Wen-Neng; Lin, Wei-Che; Cheng, Ben-Chung; Chang, Ya-Ting; Chiang, Yi-Fang; Kung, Chia-Te; Lu, Cheng-Hsien

2014-01-01

28

Intercellular Adhesion Molecule-1 (ICAM-1) in the Pathogenesis of Asthma  

NASA Astrophysics Data System (ADS)

Airway eosinophilia, epithelial desquamation, and hyperresponsiveness are characteristics of the airway inflammation underlying bronchial asthma. The contribution of intercellular adhesion molecule-1 (ICAM-1) to eosinophil migration and airway responsiveness was studied. ICAM-1 partially mediated eosinophil adhesion to endothelium in vitro and was upregulated on inflamed bronchial endothelium in vivo. ICAM-1 expression was also upregulated on inflamed airway epithelium in vitro and in vivo. In a primate model of asthma, a monoclonal antibody to ICAM-1 attenuated airway eosinophilia and hyperresponsiveness. Thus, antagonism of ICAM-1 may provide a therapeutic approach to reducing airway inflammation, hyperresponsiveness, and asthma symptoms.

Wesgner, Craig D.; Gundel, Robert H.; Reilly, Patricia; Haynes, Nancy; Letts, L. Gordon; Rothlein, Robert

1990-01-01

29

Clinical significance of serum vascular cell adhesion molecule-1 levels in patients with hepatocellular carcinoma  

Microsoft Academic Search

AIM: To evaluate the correlation between serum vascular cellular adhesion molecule-1 (VCAM-1) levels and clinicopathological features in patients with hepatocellular carcinoma (HCC). METHODS: Ninety-six patients who underwent HCC resection were recruited in the study. Preoperative serum levels of soluble VCAM-1 were measured by enzyme-linked immunosorbent assay. RESULTS: Serum VCAM-1 level in HCC patients was inversely correlated with platelet count (r=-0.431,

Joanna W. Ho; Ronnie T. Poon; Cindy S. Tong; Sheung Tat Fan

2004-01-01

30

Activation of endothelial-leukocyte adhesion molecule 1 (ELAM1) gene transcription  

Microsoft Academic Search

Leukocyte adherence to endothelium is in part mediated by the transient expression of endothelial-leukocyte adhesion molecule 1 (ELAM-1) on endothelial surfaces stimulated by tumor necrosis factor α (TNF), interleukin (IL) 1, or bacterial lipopolysaccharide (LPS). The intracellular factors controlling induction of ELAM-1 mRNA and protein are unknown. In nuclear runoff experiments with cultured human umbilical vein endothelial cells (HUVEC), the

K. F. Montgomery; P. I. Tarr; K. Bomsztyk; J. M. Harlan; T. H. Pohlman; L. Osborn; C. Hession; R. Tizard; D. Goff; C. Vassallo; R. Lobb

1991-01-01

31

Carotid atherosclerosis is associated with inflammation, malnutrition and intercellular adhesion molecule-1 in patients on continuous ambulatory peritoneal dialysis  

Microsoft Academic Search

Background. Recent evidence suggests that endothelial cell adhesion molecules may participate in the initiation and progression of atherosclerotic vascular damage. The aim of the present report was to investigate serum intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E- selectin concentrations and their probable association with atherosclerotic disease in patients on continuous ambulatory peritoneal dialysis (CAPD). Methods. Sixty-three

Aikaterini Papagianni; Elisavet Kokolina; Michalis Kalovoulos; Andreas Vainas; Chrisostomos Dimitriadis; Dimitrios Memmos

2004-01-01

32

Elevated vascular cell adhesion molecule-1 in AIDS encephalitis induced by simian immunodeficiency virus.  

PubMed Central

AIDS encephalitis is a common sequela to HIV-1 infection in humans and simian immunodeficiency virus (SIVmac) infection in macaques. Although lentiviral-infected macrophages comprise parenchymal inflammatory infiltrates in affected brain tissue, the mechanisms responsible for leukocyte trafficking to the central nervous system in AIDS are unknown. In this study, we investigated the expression of various endothelial-derived leukocyte adhesion proteins in SIVmac-induced AIDS encephalitis. Encephalitic brains from SIVmac-infected macaques, but not uninflamed brains from other SIVmac-infected animals, were found to express abundant vascular cell adhesion molecule-1 (VCAM-1) protein on the majority of arteriolar, venular, and capillary endothelial cells. Soluble VCAM-1 concentrations in cerebrospinal fluid (CSF) from encephalitic animals were increased approximately 20-fold above those from animals without AIDS encephalitis. Expression of other endothelial-related adhesion molecules, including E-selectin, P-selectin, and intercellular adhesion molecule-1 (ICAM-1), was not uniformly associated with AIDS encephalitis. Thus, the presence of VCAM-1 in both brain and CSF was uniformly associated with SIVmac-induced disease of the central nervous system, and this expression may, at least in part, influence monocyte and lymphocyte recruitment to the central nervous system during the development of AIDS encephalitis. Moreover, measurement of soluble VCAM-1 in CSF may assist in the clinical assessment of animals or people with AIDS. Images Figure 1

Sasseville, V. G.; Newman, W. A.; Lackner, A. A.; Smith, M. O.; Lausen, N. C.; Beall, D.; Ringler, D. J.

1992-01-01

33

Sophorae radix extract inhibits high glucose-induced vascular cell adhesion molecule-1 up-regulation on endothelial cell line  

Microsoft Academic Search

Background: Sophorae radix (SR) has been used for various diseases including atherosclerosis and arrhythmias. Atherosclerosis induced by hyperglycemia is an important factor in the promotion of diabetic complications. An early event in atherosclerosis is the adhesion of monocytes to endothelium via adhesion molecules. Among them, vascular cell adhesion molecule-1 (VCAM-1) expression mediates the binding of monocytes and lymphocytes to vascular

Kang-Beom Kwon; Eun-Kyung Kim; Jung-Gook Lim; Byung-Cheul Shin; Yung-Sun Song; Eun-A Seo; Ki-Young Ahn; Bong-Keun Song; Do-Gon Ryu

2004-01-01

34

Cytokines and adhesion molecules in patients with polymyalgia rheumatica  

Microsoft Academic Search

SUMMARY Serum levels of interleukin-1b (IL-1b), IL-1 receptor antagonist (IL-1ra), tumour necrosis factor alpha ( TNF-a), IL-6, soluble IL-6 receptor (sIL-6R), soluble intercellular adhesion molecule-1 (sICAM-1) and soluble E-selectin were measured in 15 patients with newly diagnosed polymyalgia rheumatica (PMR) before and after 3 months of corticosteroid therapy. Both IL-6 and IL-1ra were significantly increased in untreated PMR and remained

A. UDDHAMMAR; K.-G. SUNDQVIST; B. ELLIS

1998-01-01

35

Inflammatory and immune responses are impaired in mice deficient in intercellular adhesion molecule 1.  

PubMed Central

Gene targeting was used to produce mice deficient in intercellular adhesion molecule 1 (ICAM-1) or CD54, an immunoglobulin-like cell adhesion molecule that binds beta 2 integrins. Homozygous deficient animals develop normally, are fertile, and have a moderate granulocytosis. The nature of the mutation, RNA analysis, and immunostaining are consistent with complete loss of surface expression of ICAM-1. Deficient mice exhibit prominent abnormalities of inflammatory responses including impaired neutrophil emigration in response to chemical peritonitis and decreased contact hypersensitivity to 2,4-dinitrofluorobenzene. Mutant cells provided negligible stimulation in the mixed lymphocyte reaction, although they proliferated normally as responder cells. These mutant animals will be extremely valuable for examining the role of ICAM-1 and its counterreceptors in inflammatory disease processes and atherosclerosis. Images Fig. 1 Fig. 2

Sligh, J E; Ballantyne, C M; Rich, S S; Hawkins, H K; Smith, C W; Bradley, A; Beaudet, A L

1993-01-01

36

Intercellular adhesion molecule-1 as a drug target in asthma and rhinitis.  

PubMed

Intercellular adhesion molecule-1 (ICAM-1) is a transmembrane glycoprotein receptor of the immunoglobulin superfamily. Endothelial cells, epithelial cells, leukocytes and neutrophils are the major cells expressing ICAM-1. Ligands of ICAM-1 are macrophage adhesion ligand-1, leukocyte function-associated antigen-1 and fibrinogen (extracellular matrix protein). In normal physiological conditions, engagement of ICAM-1 receptor with immunological cells surface ligands assists in homing and trafficking of inflammatory cells to distant tissues. ICAM-1 has also long been known to mediate cell-to-cell interaction during antigen presentation and outside-in cell signalling pathways. ICAM-1-mediated elevated inflammation is implicated in asthma. On respiratory epithelial cells surface, ICAM-1 acts as natural binding site for human rhinovirus (HRV), a common cold virus that ultimately causes exacerbation of asthma. This review presents the findings on the role of ICAM-1 in the complication of asthma and in particular asthma exacerbation by HRV. PMID:24689994

Mukhopadhyay, Srirupa; Malik, Parth; Arora, Sunil K; Mukherjee, Tapan K

2014-05-01

37

Expression of vascular cell adhesion molecule-1 in fibroblastlike synoviocytes after stimulation with tumor necrosis factor.  

PubMed Central

Rapid expression of mRNA encoding vascular cell adhesion molecule-1 (VCAM-1) was induced by tumor necrosis factor (TNF) in fibroblast-like cells obtained from synovial tissue. Both alternatively spliced forms of VCAM-1 mRNA were detected by polymerase chain reaction in TNF-stimulated fibroblast-like synoviocytes. Western blotting analysis showed that two distinct proteins, reactive with an anti-VCAM-1 anti-sera, were expressed by 2 hours of TNF stimulation in both synoviocytes and human umbilical cord vein endothelial cells (HUVEC). The majority of HUVEC and synoviocytes displayed VCAM-1 surface expression after several hours of TNF stimulation. In contrast, dermal fibroblasts upregulated intercellular adhesion molecule-1 (ICAM-1) but not VCAM-1 expression in response to TNF. These results indicate that VCAM-1 and ICAM-1 expression can be differentially regulated and suggest tissue specific regulation of VCAM-1 expression. Furthermore, these findings may provide an explanation for the chronic retention and activation of long-lived lymphocytes and monocytes, which express VLA-4 (the receptor for VCAM-1), in the synovium in rheumatoid arthritis. Images Figure 1 Figure 2

Marlor, C. W.; Webb, D. L.; Bombara, M. P.; Greve, J. M.; Blue, M. L.

1992-01-01

38

Quantitative analysis of soluble cell adhesion molecules in otitis media with effusion.  

PubMed

The levels of the soluble intercellular adhesion molecule 1 (sICAM-1) and soluble granule membrane protein-140 (sGMP-140) were measured in middle ear effusions (MEEs) of otitis media (OM) with ELISA. MEEs of chronic serous and mucoid OM in children contained significantly higher levels of sICAM-1 and sGMP-140 compared with normal serum. sGMP-140 in acute and chronic OM in children was higher than in adult chronic serous OM, and in acute purulent OM higher chronic serous OM in children. Cytologic analysis showed that the mean level of sGMP-140 was significantly higher in the neutrophil dominant group than in other groups except the few cells type. sICAM-1 showed no differences among the cytologic classifications. Copious amounts of sICAM-1 and sGMP-140 in MEEs were observed in this study, and were probably the result of shedding from the cells expressed cell adhesion molecules. These cell adhesion molecules in MEEs were thought to modify the inflammatory response in OM. PMID:7521106

Himi, T; Kamimura, M; Kataura, A; Imai, K

1994-05-01

39

Drug-induced expression of intercellular adhesion molecule-1 on lesional keratinocytes in fixed drug eruption.  

PubMed Central

The mechanism(s) and the factor(s) that contribute to preferential localization of fixed drug eruption (FDE) lesions to certain skin sites remain speculative. Previous studies suggested that populations of T cells residing in the lesional epidermis may be involved in selective destruction of the epidermis in FDE. In this study, to define the earliest cellular and molecular events with potential relevance to activation of the epidermal T cells, expression of adhesion molecules on keratinocytes (KC) and vascular endothelium was examined sequentially in the lesional skin of FDE patients after challenge with the causative drug. Rapid and intense intercellular adhesion molecule-1 (ICAM-1) expression was induced on the vascular endothelium and KC as early as 1.5 hours after challenge, at which time E-selectin and vascular cell adhesion molecule-1 (VCAM-1) were not up-regulated. In vitro studies using skin organ culture showed that the lesional KC and endothelium responded more rapidly and intensely to express ICAM-1 to tumor necrosis factor-alpha or interferon-gamma compared with those in the nonlesional skin. Surprisingly, such selective induction of KC ICAM-1 restricted to the lesional skin was also observed after exposure to the causative drug alone in skin organ culture. Pretreatment of the lesional skin with anti-tumor necrosis factor completely abrogated in vitro induction of KC ICAM-1 expression by the drug. Drug-induced, TNF-alpha-dependent KC ICAM-1 expression in the lesional skin suggests that induction of ICAM-1 expression by the lesional KC after ingestion of the drug would probably provide a localized initiating stimulus for activation of the disease-associated epidermal T cells. Images Figure 1 Figure 2 Figure 3 Figure 4 Figure 5

Teraki, Y.; Moriya, N.; Shiohara, T.

1994-01-01

40

Cilostazol represses vascular cell adhesion molecule-1 gene transcription via inhibiting NF-?B binding to its recognition sequence  

Microsoft Academic Search

Cilostazol is a specific inhibitor of cAMP phosphodiesterase, which is used for treatment of ischemic symptoms of peripheral vascular disease. Although cilostazol has antiplatelet and vasodilator properties, its effect on the expression of adhesion molecules in vascular endothelium is not known. In the present investigation, we examined the effect of cilostazol on the expression of vascular cell adhesion molecule-1 (VCAM-1)

Michio Otsuki; Hiroshi Saito; Xin Xu; Satoru Sumitani; Haruhiko Kouhara; Masahiko Kurabayashi; Soji Kasayama

2001-01-01

41

Molecular architecture of a complex between an adhesion protein from the malaria parasite and intracellular adhesion molecule 1.  

PubMed

The adhesion of Plasmodium falciparum-infected erythrocytes to human tissues or endothelium is central to the pathology caused by the parasite during malaria. It contributes to the avoidance of parasite clearance by the spleen and to the specific pathologies of cerebral and placental malaria. The PfEMP1 family of adhesive proteins is responsible for this sequestration by mediating interactions with diverse human ligands. In addition, as the primary targets of acquired, protective immunity, the PfEMP1s are potential vaccine candidates. PfEMP1s contain large extracellular ectodomains made from CIDR (cysteine-rich interdomain regions) and DBL (Duffy-binding-like) domains and show extensive variation in sequence, size, and domain organization. Here we use biophysical methods to characterize the entire ?300-kDa ectodomain from IT4VAR13, a protein that interacts with the host receptor, intercellular adhesion molecule-1 (ICAM-1). We show through small angle x-ray scattering that IT4VAR13 is rigid, elongated, and monomeric. We also show that it interacts with ICAM-1 through the DBL? domain alone, forming a 1:1 complex. These studies provide a first low resolution structural view of a PfEMP1 ectodomain in complex with its ligand. They show that it combines a modular domain arrangement consisting of individual ligand binding domains, with a defined higher order architecture that exposes the ICAM-1 binding surface to allow adhesion. PMID:23297413

Brown, Alan; Turner, Louise; Christoffersen, Stig; Andrews, Katrina A; Szestak, Tadge; Zhao, Yuguang; Larsen, Sine; Craig, Alister G; Higgins, Matthew K

2013-02-22

42

MUC1 initiates a calcium signal after ligation by intercellular adhesion molecule-1.  

PubMed

The MUC1 mucin is normally restricted to the apical surface of breast epithelial cells. In tumors, it is frequently overexpressed and underglycosylated. The MUC1 peptide core mediates firm adhesion of tumor cells to adjacent cells via binding to intercellular adhesion molecule-1 (ICAM-1). There is increasing evidence that MUC1 is involved in signaling, with current reports focusing on phosphorylation of the MUC1 cytoplasmic tail after indirect or artificial modes of stimulation. ICAM-1 is the only known direct ligand of the MUC1 extracellular domain. The data presented herein show that MUC1 expressed on the surface of breast cancer cell lines or transfected 293T cells can initiate a calcium-based oscillatory signal on contact with ICAM-1-transfected NIH 3T3 cells, and we present a novel method of quantifying and comparing calcium oscillations. The MUC1-induced signal appears to be distinct from those previously described, and may involve a Src family kinase, phosphoinositol 3-kinase, phospholipase C, and lipid rafts, but not mitogen-activated protein kinase. As calcium signaling has been associated with cytoskeletal change and motility, it is possible that the functions of MUC1 include heterotypic cell-cell adhesion followed by a calcium-based promigratory signal within tumor cells, thus facilitating metastasis. PMID:15169768

Rahn, Jennifer J; Shen, Qiang; Mah, Brian K; Hugh, Judith C

2004-07-01

43

Pirfenidone induces intercellular adhesion molecule-1 (ICAM-1) down-regulation on cultured human synovial fibroblasts  

PubMed Central

Pirfenidone has been shown to modify some cytokine regulatory actions and inhibit fibroblast biochemical reactions resulting in inhibition of proliferation and collagen matrix synthesis by fibroblast. We have investigated the effect of pirfenidone on the expression of cell adhesion molecules. The synovial fibroblasts were treated with IL-1? in the presence or absence of pirfenidone (range 0–1000 ?m), and assayed for the expression of adhesion molecules such as ICAM-1 and endothelial-leucocyte adhesion molecule-1 (E-selectin) by cell ELISA. Pirfenidone significantly down-regulated the expression of ICAM-1 on cultured synovial fibroblasts in a dose-dependent manner. In contrast, expression of E-selectin was not affected. Furthermore, we examined whether pirfenidone affects the cellular binding between cultured lymphocytes and IL-1?-stimulated synovial fibroblasts by in vitro binding assay and found their mutual binding was significantly suppressed in a dose-dependent manner by pirfenidone. It is speculated that down-regulation of ICAM-1 might be one of the novel mechanisms of action of pirfenidone. These data indicate a novel mechanism of action for pirfenidone to reduce the activation of synovial fibroblasts.

Kaneko, M; Inoue, H; Nakazawa, R; Azuma, N; Suzuki, M; Yamauchi, S; Margolin, S B; Tsubota, K; Saito, I

1998-01-01

44

Soluble intercellular adhesion molecule-1 (ICAM-1) in sera and bronchoalveolar lavage (BAL) fluids of extrinsic allergic alveolitis.  

PubMed Central

ICAM-1 plays an important role in inflammatory diseases. We analysed ICAM-1 expression on BAL fluid cells and measured soluble ICAM-1 (sICAM-1) concentrations in sera and BAL fluids from patients with extrinsic allergic alveolitis (EAA). We found significantly increased cellular ICAM-1 expression on BAL fluid lymphocytes and alveolar macrophages, and significantly increased values of circulating and BAL fluid sICAM-1 in EAA patients compared with controls. Successive measurement showed prompt decrease of both sICAM-1 values in EAA patients during periods when antigen exposure was prevented. In BAL fluids from EAA patients, sICAM-1 values significantly correlated to neutrophil and ICAM-1+ lymphocyte counts. In EAA patients, circulating and BAL fluid sICAM-1 values has significant negative correlations to values of carbon monoxide diffusing capacity and to time intervals between last episode and sample collection. However, these values had significant positive correlation to values of alveolar-arterial oxygen pressure difference. In EAA, antigen exposure appears to induce cellular ICAM-1 expression on BAL fluid cells, and also appears to up-regulate shedding of ICAM-1 in the alveolar lining fluid and in the circulation. The sICAM values appear to reflect disease activity of EAA.

Shijubo, N; Imai, K; Shigehara, K; Hirasawa, M; Tsujisaki, M; Hinoda, Y; Abe, S

1995-01-01

45

Role of P-Selectin and Intercellular Adhesion Molecule1 in TNB-Induced Colitis in Rats  

Microsoft Academic Search

It has been proposed that neutrophil-endothelial cell interactions mediated by adhesion molecules are involved in the pathogenesis of inflammatory bowel disease. The objective of the present study was to determine the effects of monoclonal antibodies (MAbs) directed against endothelial adhesion molecules, P-selectin and intercellular adhesion molecule-1 (ICAM-1), in rats with colitis induced by 2,4,6-trinitrobenzene sulfonic acid (TNB). Colonic inflammation was

Norimasa Yoshida; Taiji Yamaguchi; Shuji Nakagawa; Yasunari Nakamura; Yuji Naito; Toshikazu Yoshikawa

2001-01-01

46

Mouse cells expressing human intercellular adhesion molecule-1 are susceptible to infection by coxsackievirus A21.  

PubMed Central

Competitive viral binding assays have revealed previously that coxsackievirus A21 (CAV21) and human rhinovirus 14 (HRV14) share a common cell surface receptor. More recently, intercellular adhesion molecule-1 (ICAM-1) has been identified as the cellular receptor for HRV-14. Also, anti-ICAM-1 monoclonal antibodies (MAbs) blocked infection by HRV14, CAV13, CAV18, and CAV21, suggesting that these viruses share this receptor; however, this has never been established by more direct methods. In this study we show conclusively that CAV21 binds to ICAM-1 and that MAbs directed against the N-terminal domain of the molecule inhibit this attachment. Furthermore, we show that the specific interaction between ICAM-1 and 160S CAV21 virions induces formation of 135S A particles. Finally, we show transfection of normally nonsusceptible mouse L cells with human ICAM-1 cDNA renders them susceptible to infection by CAV21.

Shafren, D R; Dorahy, D J; Greive, S J; Burns, G F; Barry, R D

1997-01-01

47

Structure, expression, and conserved physical linkage of mouse testicular cell adhesion molecule-1 (TCAM-1) gene.  

PubMed

Isolation and characterization were performed for cDNA encoding mouse testicular cell adhesion molecule-1 (TCAM-1) using 2908 bases coding for a protein having 548 amino acids (60 kDa). Mouse TCAM-1 protein was found to consist of seven domains for signal sequence, five immunoglobulin (Ig) domains, and the transmembrane plus cytoplasmic domain. TCAM-1 gene and the region linking it to growth hormone (GH) gene located downstream from the TCAM-1 gene were then analyzed. The mouse TCAM-1 gene was 11.6 kb in length with 8 exons; the same as for the 12.0 kb rat gene. The distance from the TCAM-1 to GH gene was 12.5 kb in the mouse genome, and 7.6 kb in the rat. By Northern hybridization, 3.1-kb TCAM-1 mRNA was detected in 17-day testis and would appear present in pachytene spermatocytes and round spermatids. PMID:11195349

Sakatani, S; Takahashi, R; Okuda, Y; Aizawa, A; Otsuka, A; Komatsu, A; Ono, M

2000-12-01

48

Testicular cell adhesion molecule 1 (TCAM1) is not essential for fertility  

PubMed Central

Testicular cell adhesion molecule 1 (Tcam1) is a testis-expressed gene that is evolutionarily conserved in most mammalian species. The putative location of TCAM1 on the cell surface makes it an attractive contraceptive target to study. We found that Tcam1 transcription is enriched in the adult testis, and in situ hybridization revealed that Tcam1 is expressed in pachytene to secondary spermatocytes. Immunofluorescence for TCAM1 protein showed strong expression along cell membranes of spermatocytes and weak localization to round spermatids. In light of this evidence, we hypothesized that TCAM1 interacts with an unknown receptor on the surface of Sertoli cells and that this interaction is important for germ cell-Sertoli cell interactions. However, Tcam1 knockout mice that we generated are fertile, and testis weights and sperm counts were not significantly altered. Therefore, we conclude that TCAM1 is not essential for male fertility or germ cell function in Mus musculus.

Nalam, Roopa L.; Lin, Yi-Nan; Matzuk, Martin M.

2009-01-01

49

Expression of Intercellular Adhesion Molecule1 and Vascular Cell Adhesion Molecule1 in Human Endometrial Stromal and Epithelial Cells Is Regulated by Interferon-Gamma but Not Iron  

Microsoft Academic Search

Background\\/Aims: Endometrial cells are chronically exposed to iron due to cyclic menstrual bleeding. Iron induces expression of adhesion molecules in endothelial cells. The purpose of this study was to investigate iron incorporation by human endometrial cells and to test whether iron may stimulate expression of intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1. Methods: Endometrial stromal and epithelial

Sylvie Defrère; Jacques Donnez; Pierre Moulin; Philippe Befahy; Reinaldo Gonzalez-Ramos; Jean-Christophe Lousse; Anne Van Langendonckt

2008-01-01

50

Intercellular adhesion molecule-1 is upregulated on peripheral blood T lymphocyte subsets in dual asthmatic responders.  

PubMed Central

To examine the role of adhesion molecules in T cell recruitment and activation during allergen-induced late asthmatic response (LAR), we evaluated the expression of lymphocyte function-associated antigen-1 alpha (LFA-1 alpha) and intercellular adhesion molecule-1 (ICAM-1) on peripheral blood T lymphocyte subsets from atopic asthmatic patients and their changes following allergen inhalation challenge. 12 atopic asthmatic patients were studied. Six patients showed only a single early response after allergen challenge, and six developed a dual response. At baseline, dual responders (DR) had a significantly higher expression of ICAM-1 on CD4+ and CD8+ T lymphocytes as compared with both single early responders (P < 0.005 and P < 0.02, respectively) and controls (P < 0.001, both comparisons). Allergen challenge was followed by a decrease of CD8+ ICAM-1+ T lymphocytes in all DR (P < 0.05) and of CD4+ ICAM-1+ T lymphocytes in four out of six DR, at the time of the LAR. At the same time, a significant rise in serum levels of the soluble form of ICAM-1 was observed in DR. These results suggest that peripheral blood immunoregulatory T lymphocytes are in a higher state of activation in DR as compared with early responders. The upregulation of ICAM-1 on these cells may be important in enhancing airway inflammation in patients with LAR.

De Rose, V; Rolla, G; Bucca, C; Ghio, P; Bertoletti, M; Baderna, P; Pozzi, E

1994-01-01

51

Enhanced nerve-mast cell interaction by a neuronal short isoform of cell adhesion molecule-1.  

PubMed

Close apposition of nerve and mast cells is viewed as a functional unit of neuro-immune mechanisms, and it is sustained by trans-homophilic binding of cell adhesion molecule-1 (CADM1), an Ig superfamily member. Cerebral nerve-mast cell interaction might be developmentally modulated, because the alternative splicing pattern of four (a-d) types of CADM1 transcripts drastically changed during development of the mouse cerebrum: developing cerebrums expressed CADM1b and CADM1c exclusively, while mature cerebrums expressed CADM1d additionally and predominantly. To probe how individual isoforms are involved in nerve-mast cell interaction, Neuro2a neuroblastoma cells that express CADM1c endogenously were modified to express additionally either CADM1b (Neuro2a-CADM1b) or CADM1d (Neuro2a-CADM1d), and they were cocultured with mouse bone marrow-derived mast cells (BMMCs) and BMMC-derived cell line IC-2 cells, both of which expressed CADM1c. BMMCs were found to adhere to Neuro2a-CADM1d neurites more firmly than to Neuro2a-CADM1b neurites when the adhesive strengths were estimated from the femtosecond laser-induced impulsive forces minimally required for detaching BMMCs. GFP-tagging and crosslinking experiments revealed that the firmer adhesion site consisted of an assembly of CADM1d cis-homodimers. When Neuro2a cells were specifically activated by histamine, intracellular Ca(2+) concentration was increased in 63 and 38% of CADM1c-expressing IC-2 cells that attached to the CADM1d assembly site and elsewhere, respectively. These results indicate that CADM1d is a specific neuronal isoform that enhances nerve-mast cell interaction, and they suggest that nerve-mast cell interaction may be reinforced as the brain grows mature because CADM1d becomes predominant. PMID:21482734

Hagiyama, Man; Furuno, Tadahide; Hosokawa, Yoichiroh; Iino, Takanori; Ito, Takeshi; Inoue, Takao; Nakanishi, Mamoru; Murakami, Yoshinori; Ito, Akihiko

2011-05-15

52

Association of intercellular adhesion molecule?1 gene polymorphism with coronary heart disease.  

PubMed

Intercellular adhesion molecule?1 (ICAM?1) is an important adhesion molecule that has a crucial role in lymphocyte migration and atherosclerosis pathogenesis activation. The aim of the present study was to explore the association between the rs5498 polymorphism of the ICAM?1 gene and coronary heart disease (CHD). The rs5498 polymorphism of the ICAM?1 gene was detected using polymerase chain reaction?restriction fragment length polymorphism in 674 patients with CHD and 779 control subjects. The results showed that the frequency of the G allele was significantly higher in patients with CHD than that in controls (29.1 vs. 23.3%; P<0.001). The frequency of the AG+GG genotypes was higher in patients with CHD than that in controls (49.7 vs. 40.8%; P=0.001). Multiple logistic regression analysis showed that AG+GG was an independent risk factor for CHD (odds ratio, 1.919; 95% confidence intervals, 1.471?2.503; P<0.001). For males, the frequencies of the G allele and AG+GG genotype were also higher in patients with CHD than those in control subjects (frequency of G allele, 29.9 vs. 22.7%; P<0.001; frequency of AG+GG genotype, 50.6 vs. 40.3%; P=0.001). For females, no significant differences in genotype or allele distribution were observed between the two groups. In conclusion, it was demonstrated in the present study that the rs5498 polymorphism of the ICAM?1 gene was associated with CHD in males. Males with the G allele (AG and GG genotype) may therefore have a higher risk for CHD than those with the AA genotype. PMID:24993975

Luo, Jun-Yi; Ma, Yi-Tong; Xie, Xiang; Yang, Yi-Ning; Li, Xiao-Mei; Ma, Xiang; Yu, Zixiang; Chen, Bang-Dang; Liu, Fen

2014-09-01

53

Intercellular adhesion molecule-1 (ICAM-1) expression is upregulated in autoimmune murine lupus nephritis.  

PubMed Central

Intercellular adhesion molecule-1 (ICAM-1) is a cell-surface protein regulating interactions among immune cells. To determine whether altered expression of ICAM-1 occurs in autoimmune lupus nephritis, we studied ICAM-1 expression in kidneys of normal and autoimmune MRL-lpr and (NZBX NZW)F1 (NZB/W) mice. By immunoperoxidase staining, ICAM-1 is constitutively expressed at low levels in proximal tubules (PT), endothelium and interstitial cells in normal C3H/FeJ mice. In nephritic MRL-lpr and NZB/W kidneys, staining for ICAM-1 is increased in the PT, particularly in the brush border, and is prominent in the glomerular mesangium and the endothelium of large vessels. By Western blot analysis, ICAM-1 is not detected in the urine of normal BALB/c and C3H/FeJ or autoimmune MRL-lpr. By Northern blot analysis, nephritic MRL-lpr and NZB/W have a two- to fivefold increase in steady state levels of ICAM-1 transcripts in the kidney as compared with normal or prenephritic mice. This is paralleled by an increase in MHC class II transcripts. In cultured PT cells, ICAM-1 is expressed at basal levels in PT and is increased by the cytokines interferon-gamma, IL-1 alpha, and TNF-alpha. Thus cytokine-mediated upregulation of ICAM-1 in lupus nephritis may promote interaction of immune cells with renal tissue. The predominant apical expression of ICAM-1 opposite to the basolateral Ia expression suggests a novel role for this adhesion molecule in PT. Images Figure 1 Figure 2 Figure 3 Figure 6 Figure 7

Wuthrich, R. P.; Jevnikar, A. M.; Takei, F.; Glimcher, L. H.; Kelley, V. E.

1990-01-01

54

The role of intercellular adhesion molecule-1 in chronic airway inflammation.  

PubMed

We have examined the role of intercellular adhesion molecule-1 (ICAM-1) in chronic airway inflammation and airway hyperresponsiveness in a primate model of asthma. Airway cellular composition was assessed by bronchoalveolar lavage (BAL) and airway responsiveness was measured as the bronchoconstrictor response to inhaled methacholine. In animals with chronic airway inflammation (increased BAL eosinophils) and sustained airway hyperresponsiveness, a 7 day dosing scheme with a murine anti-human ICAM-1 monoclonal antibody (R6.5, 2 mg/kg/day; i.v.) did not reduce the existing airway inflammation or airway hyperresponsiveness. In contrast, a similar dosing scheme with dexamethasone (0.2 mg/kg/day, i.m.) was found to significantly reduce both the airway eosinophilia and hyperresponsiveness. However, one week after cessation of dexamethasone treatment, the airway inflammation and hyperresponsiveness returned to pre-treatment levels. In further experiments where animals were first treated with dexamethasone (7 days) followed by a 7 day treatment with R6.5, the reoccurrence of airway inflammation and subsequent increase in airway responsiveness was prevented. We conclude that the efficacy of ICAM-1 is primarily associated with inhibition of the influx of inflammatory cells into the airways and subsequent reduction in airway responsiveness. These data suggest that in lungs with pre-existing inflammation the modulation of ICAM-1 following treatment with glucocorticoids may be a novel and more selective long-term treatment for control of the chronic airway inflammation and hyperresponsiveness associated with bronchial asthma. PMID:1352734

Gundel, R H; Wegner, C D; Torcellini, C A; Letts, L G

1992-05-01

55

Association of intercellular adhesion molecule 1 (ICAM1) with diabetes and diabetic nephropathy  

PubMed Central

Diabetes and diabetic nephropathy are complex diseases affected by genetic and environmental factors. Identification of the susceptibility genes and investigation of their roles may provide useful information for better understanding of the pathogenesis and for developing novel therapeutic approaches. Intercellular adhesion molecule 1 (ICAM1) is a cell surface glycoprotein expressed on endothelial cells and leukocytes in the immune system. The ICAM1 gene is located on chromosome 19p13 within the linkage region of diabetes. In the recent years, accumulating reports have implicated that genetic polymorphisms in the ICAM1 gene are associated with diabetes and diabetic nephropathy. Serum ICAM1 levels in diabetes patients and the icam1 gene expression in kidney tissues of diabetic animals are increased compared to the controls. Therefore, ICAM1 may play a role in the development of diabetes and diabetic nephropathy. In this review, we present genomic structure, variation, and regulation of the ICAM1 gene, summarized genetic and biological studies of this gene in diabetes and diabetic nephropathy and discussed about the potential application using ICAM1 as a biomarker and target for prediction and treatment of diabetes and diabetic nephropathy.

Gu, Harvest F.; Ma, Jun; Gu, Karolin T.; Brismar, Kerstin

2013-01-01

56

Carcinoembryonic antigen-related cell adhesion molecule 1 inhibits proximal TCR signaling by targeting ZAP-70.  

PubMed

The long cytoplasmic tail (CT) isoforms of carcinoembryonic Ag-related cell adhesion molecule 1 (CEACAM1) are expressed on activated human T cells and possess two ITIM motifs in the CT. These isoforms of CEACAM1 are inhibitory for T cell responses initiated by the TCR/CD3 complex with the inhibition dependent upon the ITIMs of CEACAM1 and Src homology 2 domain-containing phosphatase 1 (SHP-1). However, the mechanism by which this inhibition occurs in T cells is unknown. We demonstrate here that the Src family kinase, Lck, and the ability of CEACAM1 to bind homophilically are required for the ITIM phosphorylation of CEACAM1 that is a prerequisite for CEACAM1 association with SHP-1. We further show that CEACAM1 associates with and recruits SHP-1 to the TCR/CD3 complex leading to decreased phosphorylation of CD3-zeta and ZAP-70 and consequently decreased activation of the elements downstream of ZAP-70. This is physiologically relevant because extinction of SHP-1 expression or blockade of homophilic binding by CEACAM1 using a Fab that specifically recognizes the homophilic binding region of human CEACAM1 increases the cytolytic function initiated by the TCR/CD3 complex. These studies show that long CT isoforms of CEACAM1 orchestrate an inhibitory program that abrogates extremely proximal events downstream of the TCR/CD3 complex by focusing on the activation of ZAP-70. PMID:18424730

Chen, Zhangguo; Chen, Lanfen; Qiao, Shuo-Wang; Nagaishi, Takashi; Blumberg, Richard S

2008-05-01

57

Vascular cell adhesion molecule 1: contrasting transcriptional control mechanisms in muscle and endothelium.  

PubMed Central

Interaction between vascular cell adhesion molecule 1 (VCAM-1), which appears on the surface of endothelial cells in response to inflammation, and its integrin counter receptor, alpha 4 beta 1, on immune cells is responsible for targeting these immune cells to cytokine-stimulated endothelium. In addition to its role in the immune system, VCAM-1 is also expressed in a developmentally specific pattern on differentiating skeletal muscle, where it mediates cell-cell interactions important for myogenesis through interaction with alpha 4 beta 1. In contrast to endothelium, there is high basal expression of VCAM-1 in skeletal muscle cells and the expression is not cytokine-responsive. Here, we examine the molecular basis for these contrasting patterns of expression in muscle and endothelium, using VCAM-1 promoter constructs in a series of transfection assays. In endothelial cells, octamer binding sites act as silencers that prevent VCAM-1 expression in unstimulated cells. Tumor necrosis factor alpha overcomes the negative effects of these octamers and activates the promoter through two adjacent NF-kappa B binding sites. In muscle cells, a position-specific enhancer located between bp -21 and -5 overrides the effect of other promoter elements, resulting in constitutive VCAM-1 expression. A nuclear protein binds the position-specific enhancer in muscle but not endothelial cells; thus the pattern of expression of this protein could control enhancer activity. Images Fig. 1 Fig. 3 Fig. 4

Iademarco, M F; McQuillan, J J; Dean, D C

1993-01-01

58

Active Site Formation, Not Bond Kinetics, Limits Adhesion Rate between Human Neutrophils and Immobilized Vascular Cell Adhesion Molecule 1  

PubMed Central

Abstract The formation of receptor ligand bonds at the interface between different cells and between cells and substrates is a widespread phenomenon in biological systems. Physical measurements of bond formation rates between cells and substrates have been exploited to increase our understanding of the biophysical mechanisms that regulate bond formation at interfaces. Heretofore, these measurements have been interpreted in terms of simple bimolecular reaction kinetics. Discrepancies between this simple framework and the behavior of neutrophils adhering to surfaces expressing vascular cell adhesion molecule 1 (VCAM-1) motivated the development of a new kinetic framework in which the explicit formation of active bond formation sites (reaction zones) are a prerequisite for bond formation to occur. Measurements of cells interacting with surfaces having a wide range of VCAM-1 concentrations, and for different durations of contact, enabled the determination of novel kinetic rate constants for the formation of reaction zones and for the intrinsic bond kinetics. Comparison of these rates with rates determined previously for other receptor-ligand pairs points to a predominant role of extrinsic factors such as surface topography and accessibility of active molecules to regions of close contact in determining forward rates of bond formation at cell interfaces.

Waugh, Richard E.; Lomakina, Elena B.

2009-01-01

59

Vascular endothelial platelet endothelial cell adhesion molecule 1 (PECAM-1) regulates advanced metastatic progression  

PubMed Central

Most patients who die from cancer succumb to treatment-refractory advanced metastatic progression. Although the early stages of tumor metastasis result in the formation of clinically silent micrometastatic foci, its later stages primarily reflect the progressive, organ-destructive growth of already advanced metastases. Early-stage metastasis is regulated by multiple factors within tumor cells as well as by the tumor microenvironment (TME). In contrast, the molecular determinants that control advanced metastatic progression remain essentially uncharacterized, precluding the development of therapies targeted against it. Here we show that the TME, functioning in part through platelet endothelial cell adhesion molecule 1 (PECAM-1), drives advanced metastatic progression and is essential for progression through its preterminal end stage. PECAM-1–KO and chimeric mice revealed that its metastasis-promoting effects are mediated specifically through vascular endothelial cell (VEC) PECAM-1. Anti–PECAM-1 mAb therapy suppresses both end-stage metastatic progression and tumor-induced cachexia in tumor-bearing mice. It reduces proliferation, but not angiogenesis or apoptosis, within advanced tumor metastases. Because its antimetastatic effects are mediated by binding to VEC rather than to tumor cells, anti–PECAM-1 mAb appears to act independently of tumor type. A modified 3D coculture assay showed that anti–PECAM-1 mAb inhibits the proliferation of PECAM-1–negative tumor cells by altering the concentrations of secreted factors. Our studies indicate that a complex interplay between elements of the TME and advanced tumor metastases directs end-stage metastatic progression. They also suggest that some therapeutic interventions may target late-stage metastases specifically. mAb-based targeting of PECAM-1 represents a TME-targeted therapeutic approach that suppresses the end stages of metastatic progression, until now a refractory clinical entity.

DeLisser, Horace; Liu, Yong; Desprez, Pierre-Yves; Thor, Ann; Briasouli, Paraskevei; Handumrongkul, Chakrapong; Wilfong, Jonathon; Yount, Garret; Nosrati, Mehdi; Fong, Sylvia; Shtivelman, Emma; Fehrenbach, Melane; Cao, Gaoyuan; Moore, Dan H.; Nayak, Shruti; Liggitt, Denny; Kashani-Sabet, Mohammed; Debs, Robert

2010-01-01

60

Interaction of Intercellular Adhesion Molecule 1 (ICAM1) Polymorphisms and Environmental Tobacco Smoke on Childhood Asthma.  

PubMed

Asthma is a chronic disease that is particularly common in children. The association between polymorphisms of the gene encoding intercellular adhesion molecule 1 (ICAM1) and gene-environment interactions with childhood asthma has not been fully investigated. A cross-sectional study was undertaken to investigate these associations among children in Taiwan. The effects of two functional single-nucleotide polymorphisms (SNPs) of ICAM1, rs5491 (K56M) and rs5498 (K469E), and exposure to environmental tobacco smoke (ETS) were studied. Two hundred and eighteen asthmatic and 877 nonasthmatic children were recruited from elementary schools. It was found that the genetic effect of each SNP was modified by the other SNP and by exposure to ETS. The risk of asthma was higher for children carrying the rs5491 AT or TT genotypes and the rs5498 GG genotype (odds ratio = 1.68, 95% confidence interval 1.09-2.59) than for those with the rs5491 AA and rs5498 AA or AG genotypes (the reference group). The risk for the other two combinations of genotypes did not differ significantly from that of the reference group (p of interaction = 0.0063). The two studied ICAM1 SNPs were associated with childhood asthma among children exposed to ETS, but not among those without ETS exposure (p of interaction = 0.05 and 0.01 for rs5491 and rs5498, respectively). Both ICAM1 and ETS, and interactions between these two factors are likely to be involved in the development of asthma in childhood. PMID:24955718

Li, Yu-Fen; Lin, Che-Chen; Tai, Chien-Kuo

2014-01-01

61

Interaction of Intercellular Adhesion Molecule 1 (ICAM1) Polymorphisms and Environmental Tobacco Smoke on Childhood Asthma  

PubMed Central

Asthma is a chronic disease that is particularly common in children. The association between polymorphisms of the gene encoding intercellular adhesion molecule 1 (ICAM1) and gene-environment interactions with childhood asthma has not been fully investigated. A cross-sectional study was undertaken to investigate these associations among children in Taiwan. The effects of two functional single-nucleotide polymorphisms (SNPs) of ICAM1, rs5491 (K56M) and rs5498 (K469E), and exposure to environmental tobacco smoke (ETS) were studied. Two hundred and eighteen asthmatic and 877 nonasthmatic children were recruited from elementary schools. It was found that the genetic effect of each SNP was modified by the other SNP and by exposure to ETS. The risk of asthma was higher for children carrying the rs5491 AT or TT genotypes and the rs5498 GG genotype (odds ratio = 1.68, 95% confidence interval 1.09–2.59) than for those with the rs5491 AA and rs5498 AA or AG genotypes (the reference group). The risk for the other two combinations of genotypes did not differ significantly from that of the reference group (p of interaction = 0.0063). The two studied ICAM1 SNPs were associated with childhood asthma among children exposed to ETS, but not among those without ETS exposure (p of interaction = 0.05 and 0.01 for rs5491 and rs5498, respectively). Both ICAM1 and ETS, and interactions between these two factors are likely to be involved in the development of asthma in childhood.

Li, Yu-Fen; Lin, Che-Chen; Tai, Chien-Kuo

2014-01-01

62

Intercellular adhesion molecule 1 promotes HIV-1 attachment but not fusion to target cells.  

PubMed

Incorporation of intercellular adhesion molecule 1 (ICAM-1) into HIV-1 particles is known to markedly enhance the virus binding and infection of cells expressing lymphocyte function-associated antigen-1 (LFA-1). At the same time, ICAM-1 has been reported to exert a less pronounced effect on HIV-1 fusion with lymphoid cells. Here we examined the role of ICAM-1/LFA-1 interactions in productive HIV-1 entry into lymphoid cells using a direct virus-cell fusion assay. ICAM-1 promoted HIV-1 attachment to cells in a temperature-dependent manner. It exerted a marginal effect on virus binding in the cold, but enhanced binding up to 4-fold at physiological temperature. ICAM-1-independent attachment in the cold was readily reversible upon subsequent incubation at elevated temperature, whereas ICAM-1-bearing particles were largely retained by cells. The better virus retention resulted in a proportional increase in HIV-1 internalization and fusion, suggesting that ICAM-1 did not specifically accelerate endocytosis or fusion steps. We also measured the rates of CD4 engagement, productive endocytosis and HIV-endosome fusion using specific fusion inhibitors. These rates were virtually independent of the presence of ICAM-1 in viral particles. Importantly, irrespective of the presence of ICAM-1, HIV-1 escaped from the low temperature block, which stopped virus endocytosis and fusion, much later than from a membrane-impermeant fusion inhibitor targeting surface-accessible particles. This result, along with the complete inhibition of HIV-1 fusion by a small molecule dynamin inhibitor, implies this virus enters lymphoid cells used in this study via endocytosis and that this pathway is not altered by the viral ICAM-1. Our data highlight the role of ICAM-1 in stabilizing the HIV-1 attachment to LFA-1 expressing cells, which leads to a proportional enhancement of the receptor-mediated uptake and fusion with endosomes. PMID:22970312

Kondo, Naoyuki; Melikyan, Gregory B

2012-01-01

63

Intracellular Adhesion Molecule 1 Plays a Key Role in Acquired Immunity to Salmonellosis  

PubMed Central

This study investigated the role of intracellular adhesion molecule 1 (ICAM-1) during Salmonella enterica serovar Typhimurium infection of mice. We show that ICAM-1 is expressed in and around granulomas on day 4 of infection in wild-type mice. However, when naive ICAM-1?/? mice were challenged with a sublethal dose of serovar Typhimurium, there were no detectable differences in systemic bacterial burden over the first 9 days of infection compared to wild-type control mice. When mice were immunized with the S. enterica serovar Typhimurium vaccine strain SL2361 and then challenged with the virulent S. enterica serovar Typhimurium strain C5, 100% of the ICAM-1?/? mice succumbed to infection, compared to 30% of wild-type mice. T-cell responses, as measured by activation via interleukin-2 production, as well as antibody responses were comparable in the ICAM-1?/? and wild-type mice. Following challenge, counts in organs were significantly higher in the ICAM-1?/? mice, and histological examination of organs showed pathological differences. Strain SL3261-immunized wild-type mice had cellular infiltrate and normal granuloma formation in the liver and spleen on days 5 and 10 after challenge with strain C5. ICAM-1?/? mice had a similar infiltrate on day 5, whereas on day 10 the infiltrate was more widespread and there were fewer macrophages associated with the granulomas. High circulating levels of tumor necrosis factor alpha and gamma interferon, as well as a high burden of strain C5 in the blood, accompanied the differences in histopathology. In this study we show that ICAM-1 plays a critical role during rechallenge of immunized mice with virulent S. enterica serovar Typhimurium.

Clare, Simon; Goldin, Robert; Hale, Christine; Aspinall, Richard; Simmons, Cameron; Mastroeni, Pietro; Dougan, Gordon

2003-01-01

64

Intercellular Adhesion Molecule 1 Promotes HIV-1 Attachment but Not Fusion to Target Cells  

PubMed Central

Incorporation of intercellular adhesion molecule 1 (ICAM-1) into HIV-1 particles is known to markedly enhance the virus binding and infection of cells expressing lymphocyte function-associated antigen-1 (LFA-1). At the same time, ICAM-1 has been reported to exert a less pronounced effect on HIV-1 fusion with lymphoid cells. Here we examined the role of ICAM-1/LFA-1 interactions in productive HIV-1 entry into lymphoid cells using a direct virus-cell fusion assay. ICAM-1 promoted HIV-1 attachment to cells in a temperature-dependent manner. It exerted a marginal effect on virus binding in the cold, but enhanced binding up to 4-fold at physiological temperature. ICAM-1-independent attachment in the cold was readily reversible upon subsequent incubation at elevated temperature, whereas ICAM-1-bearing particles were largely retained by cells. The better virus retention resulted in a proportional increase in HIV-1 internalization and fusion, suggesting that ICAM-1 did not specifically accelerate endocytosis or fusion steps. We also measured the rates of CD4 engagement, productive endocytosis and HIV-endosome fusion using specific fusion inhibitors. These rates were virtually independent of the presence of ICAM-1 in viral particles. Importantly, irrespective of the presence of ICAM-1, HIV-1 escaped from the low temperature block, which stopped virus endocytosis and fusion, much later than from a membrane-impermeant fusion inhibitor targeting surface-accessible particles. This result, along with the complete inhibition of HIV-1 fusion by a small molecule dynamin inhibitor, implies this virus enters lymphoid cells used in this study via endocytosis and that this pathway is not altered by the viral ICAM-1. Our data highlight the role of ICAM-1 in stabilizing the HIV-1 attachment to LFA-1 expressing cells, which leads to a proportional enhancement of the receptor-mediated uptake and fusion with endosomes.

Kondo, Naoyuki; Melikyan, Gregory B.

2012-01-01

65

Effects of the prostaglandin I 2 analogue, beraprost sodium, on vascular cell adhesion molecule-1 expression in human vascular endothelial cells and circulating vascular cell adhesion molecule-1 level in patients with type 2 diabetes mellitus  

Microsoft Academic Search

Beraprost sodium is an orally active prostaglandin (PG)I2 analogue, which has antiplatelet and vasodilating properties. In this study, we investigated the effects of beraprost on the expression of vascular cell adhesion molecule-1 (VCAM-1), one of the key molecules involved in atherosclerosis, in cultured vascular endothelial cells. In addition, we examined the effects of beraprost on circulating VCAM-1 level and atherosclerosis

K. Goya; M. Otsuki; X. Xu; S. Kasayama

2003-01-01

66

Tetraspanins CD81 and CD82 facilitate ?4?1-mediated adhesion of human erythroblasts to vascular cell adhesion molecule-1.  

PubMed

The proliferation and terminal differentiation of erythroid progenitors occurs in human bone marrow within erythroblastic islands, specialised structures consisting of a central macrophage surrounded by developing erythroid cells. Many cell-cell and cell-matrix adhesive interactions maintain and regulate the co-ordinated daily production of reticulocytes. Erythroid cells express only one integrin, ?4?1, throughout differentiation, and its interactions with both macrophage Vascular Cell Adhesion Molecule-1 and with extracellular matrix fibronectin are critical for erythropoiesis. We observed that proerythroblasts expressed a broad tetraspanin phenotype, and investigated whether any tetraspanin could modulate integrin function. A specific association between ?4?1 and CD81, CD82 and CD151 was demonstrated by confocal microscopy and co-immune precipitation. We observed that antibodies to CD81 and CD82 augmented adhesion of proerythroblasts to Vascular Cell Adhesion Molecule-1 but not to the fibronectin spliceoforms FnIII12-IIICS-15 and FnIII12-15. In contrast, different anti-CD151 antibodies augmented or inhibited adhesion of proerythroblasts to Vascular Cell Adhesion Molecule-1 and the fibronectin spliceoform FnIII12-IIICS-15 but not to FnIII12-15. These results strongly suggest that tetraspanins have a functional role in terminal erythropoiesis by modulating interactions of erythroblast ?4?1 with both macrophages and extracellular matrix. PMID:23704882

Spring, Frances A; Griffiths, Rebecca E; Mankelow, Tosti J; Agnew, Christopher; Parsons, Stephen F; Chasis, Joel A; Anstee, David J

2013-01-01

67

Activated endothelium binds lymphocytes through a novel binding site in the alternately spliced domain of vascular cell adhesion molecule-1  

PubMed Central

Vascular cell adhesion molecule-1 (VCAM-1) is induced on endothelial cells by inflammatory cytokines, and binds mononuclear leukocytes through the integrin very late antigen-4 (VLA-4) (alpha 4 beta 1). This adhesion pathway has been implicated in a diverse group of physiological and pathological processes, including B cell development, leukocyte activation and recruitment to sites of inflammation, atherosclerosis, and tumor cell metastasis. The major form of VCAM-1 (VCAM-7D) has seven extracellular immunoglobulin (Ig)-like domains, of which the three NH2-terminal domains (domains 1-3) are similar in amino acid sequence to domains 4-6. By functional analysis of VCAM-7D relative to VCAM-6D (a minor 6-domain form of VCAM-1 in which domain 4 is deleted because of alternative splicing), and chimeric constructs between VCAM-1 and its structural relative intercellular adhesion molecule-1 (ICAM-1), we show that either the first or the homologous fourth domain of VCAM-1 is required for VLA-4-dependent adhesion. Either of these binding sites can function in the absence of the other. When both are present, cell binding activity is increased relative to monovalent forms of the molecule. The homologous binding regions appear to have originated by internal duplication of a portion of a monovalent ancestral gene, before the mammalian radiation. Thus VCAM-1 exemplifies evolution of a functionally bivalent cell-cell adhesion molecule by intergenic duplication. We have also produced a new class of anti-VCAM- 1 monoclonal antibodies that block domain 4-dependent adhesion, and demonstrate that both binding sites participate in the adhesion function of VCAM-1 on endothelial cells in vitro. Therefore both sites must be blocked in clinical, animal, or in vitro studies depending on the use of anti-VCAM-1 antibodies to inactivate the VCAM-1/VLA-4 adhesion pathway.

1992-01-01

68

Monocyte attachment to activated human vascular endothelium in vitro is mediated by leukocyte adhesion molecule-1 (L-selectin) under nonstatic conditions  

PubMed Central

The receptors that mediate monocyte adhesion to cytokine-stimulated endothelial monolayers were assessed using a nonstatic (rotating) cell- attachment assay. In this system, leukocyte adhesion molecule-1 (LAM-1) (L-selectin) mediated a major portion (87 +/- 15% at 37 degrees C) of monocyte attachment to activated endothelium. mAb blocking of endothelial leukocyte adhesion molecule-1 (41% inhibition), CD18 (36%), and vascular cell adhesion molecule-1 (25%) function had lesser effects on attachment. These results suggest that LAM-1 may serve an important role in monocyte attachment to endothelium at sites of inflammation.

1992-01-01

69

Arsenite enhances tumor necrosis factor-{alpha}-induced expression of vascular cell adhesion molecule-1  

SciTech Connect

Epidemiological studies demonstrated a high association of vascular diseases with arsenite exposure. We hypothesize that arsenite potentiates the effect of proinflammatory cytokines on vascular endothelial cells, and hence contributes to atherosclerosis. In this study, we investigated the effect of arsenite and its induction of glutathione (GSH) on vascular cell adhesion molecule-1 (VCAM-1) protein expression in human umbilical vein endothelial cells (HUVECs) in response to tumor necrosis factor-{alpha} (TNF-{alpha}), a typical proinflammatory cytokine. Our study demonstrated that arsenite pretreatment potentiated the TNF-{alpha}-induced VCAM-1 expression with up-regulations of both activator protein-1 (AP-1) and nuclear factor-{kappa}B (NF-{kappa}B). To elucidate the role of GSH in regulation of AP-1, NF-{kappa}B, and VCAM-1 expression, we employed L-buthionine (S,R)-sulfoximine (BSO), a specific {gamma}-glutamylcysteine synthetase ({gamma}-GCS) inhibitor, to block intracellular GSH synthesis. Our investigation revealed that, by depleting GSH, arsenite attenuated the TNF-{alpha}-induced VCAM-1 expression as well as a potentiation of AP-1 and an attenuation of NF-{kappa}B activations by TNF-{alpha}. Moreover, we found that depletion of GSH would also attenuate the TNF-{alpha}-induced VCAM-1 expression with a down-regulation of the TNF-{alpha}-induced NF-{kappa}B activation and without significant effect on AP-1. On the other hand, the TNF-{alpha}-induced VCAM-1 expression could be completely abolished by inhibition of AP-1 or NF-{kappa}B activity, suggesting that activation of both AP-1 and NF-{kappa}B was necessary for VCAM-1 expression. In summary, we demonstrate that arsenite enhances the TNF-{alpha}-induced VCAM-1 expression in HUVECs via regulation of AP-1 and NF-{kappa}B activities in a GSH-sensitive manner. Our present study suggested a potential mechanism for arsenite in the induction of vascular inflammation and vascular diseases via modulating the actions of proinflammatory cytokines.

Tsou, T.-C. [Division of Environmental Health and Occupational Medicine, National Health Research Institutes, 100 Shih-Chuan 1st Road, Kaohsiung 807, Taiwan (China)]. E-mail: tctsou@nhri.org.tw; Yeh, Szu Ching [Division of Environmental Health and Occupational Medicine, National Health Research Institutes, 100 Shih-Chuan 1st Road, Kaohsiung 807, Taiwan (China); Tsai, E.-M. [Department of Obstetrics and Gynecology, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan (China); Department of Obstetrics and Gynecology, Kaohsiung Medical University Chung-Ho Memorial Hospital, Kaohsiung, Taiwan (China); Tsai, F.-Y. [Division of Environmental Health and Occupational Medicine, National Health Research Institutes, 100 Shih-Chuan 1st Road, Kaohsiung 807, Taiwan (China); Chao, H.-R. [Department of Environmental and Safety Health Engineering, Chung Hwa College of Medical Technology, Tainan, Taiwan (China); Chang, Louis W. [Division of Environmental Health and Occupational Medicine, National Health Research Institutes, 100 Shih-Chuan 1st Road, Kaohsiung 807, Taiwan (China)

2005-11-15

70

Soluble platelet-endothelial cell adhesion molecule-1, a biomarker of ventilator-induced lung injury  

PubMed Central

Introduction Endothelial cell injury is an important component of acute lung injury. Platelet-endothelial cell adhesion molecule-1 (PECAM1) is a transmembrane protein that connects endothelial cells to one another and can be detected as a soluble, truncated protein (sPECAM1) in serum. We hypothesized that injurious mechanical ventilation (MV) leads to shedding of PECAM1 from lung endothelial cells resulting in increasing sPECAM1 levels in the systemic circulation. Methods We studied 36 Sprague–Dawley rats in two prospective, randomized, controlled studies (healthy and septic) using established animal models of ventilator-induced lung injury. Animals (n?=?6 in each group) were randomized to spontaneous breathing or two MV strategies: low tidal volume (VT) (6 ml/kg) and high-VT (20 ml/kg) on 2 cmH2O of positive end-expiratory pressure (PEEP). In low-VT septic animals, 10 cmH2O of PEEP was applied. We performed pulmonary histological and physiological evaluation and measured lung PECAM1 protein content and serum sPECAM1 levels after four hours ventilation period. Results High-VT MV caused severe lung injury in healthy and septic animals, and decreased lung PECAM1 protein content (P?

2014-01-01

71

Fosinopril decreases levels of soluble vascular cell adhesion molecule-1 in borderline hypertensive type II diabetic patients with microalbuminuria  

Microsoft Academic Search

Angiotensin converting enzyme inhibitors (ACE-I) are a mainstay for the treatment of heart failure, and of diabetic microalbuminuria. Recently ACE-I have been found to decrease plasma levels of circulating vascular cell adhesion molecule-1 (cVCAM-1) in patients with congestive heart failure. As increased cVCAM-1 levels are pathognomonic for diabetics with microangiopathy, we investigated the effects of ACE-I on plasma levels of

Slobodan Gasic; Oswald F. Wagner; Peter Fasching; Christine Ludwig; Mario Veitl; Stylianos Kapiotis; Bernd Jilma

1999-01-01

72

Carcinoembryonic Antigen-Related Cellular Adhesion Molecule 1 Isoforms Alternatively Inhibit and Costimulate Human T Cell Function1  

Microsoft Academic Search

Carcinoembryonic Ag-related cellular adhesion molecule 1 (CEACAM1) represents a group of transmembrane protein isoforms that consist of variable numbers of extracellular Ig-like domains together with either a long cytoplasmic (cyt) tail containing two immunoreceptor tyrosine-based inhibitory motifs or a unique short cyt tail. Although CEACAM1 has been reported to be ex- pressed on the surface of T lymphocytes upon activation,

Daohong Chen; Hideki Iijima; Takashi Nagaishi; Atsushi Nakajima; Sara Russell; Raktima Raychowdhury; Victor Morales; Christopher E. Rudd; Nalan Utku; Richard S. Blumberg

73

Differential Susceptibility of Cultured Human Melanoma Cell Lines to Enhancement by Retinole Acid of Intercellular Adhesion Molecule 1 Expression1  

Microsoft Academic Search

The potential role of intercellular adhesion molecule 1 (ICAM-1) in the biology of human melanoma cells has stimulated interest in the characterization of its modulation. The present study has shown that the differentiating agent retinole acid (RA) up-regulates ICAM-1 expres sion by melanoma cells in a dose- and time-dependent fashion. The enhancement of ICAM-1 cell surface expression is paralleled by

Zhigang Wang; Yan Cao; Claudio M. D'Urso; Soldano Terrone

74

Elevated soluble cellular adhesion molecules in subjects with low HDL-cholesterol.  

PubMed

The purpose of this study was to investigate whether the expression of cellular adhesion molecules (CAMs) is enhanced in individuals with low HDL cholesterol (HDL-C). Plasma levels of soluble vascular cell adhesion molecule-1 (sVCAM-1), intercellular adhesion molecule-1 (sICAM-1), and E-selectin (sE-selectin) were measured in subjects with low (below the 10th percentile for the Italian population), average, or high (above the 90th percentile) HDL-C. Average sICAM-1 and sE-selectin levels were significantly higher in two groups of 65 individuals with low HDL levels, either hyperlipidemic (320.5+/-16.0 and 61.4+/-3.5 ng/mL) or normolipidemic (309.6+/-13.0 and 60.0+/-2.7 ng/mL), than in subjects with average HDL levels, either hyperlipidemic (267.0+/-10.1 and 50.4+/-2.8 ng/mL) or normolipidemic (257.9+/-5.4 and 51.1+/-2.4 ng/mL), or with high HDL levels (254.8+/-10.2 and 52.5+/-3.2 ng/mL). No significant difference was found in the plasma sVCAM-1 concentration. HDL-C was inversely correlated with sICAM-1 and sE-selectin in the low-HDL subjects (r(2)=0.087 and 0.035, P=0.0007 and 0.033, respectively), but not in individuals with normal or elevated HDL-C (r(2)=0.012 and 0.006). A fenofibrate-induced increase of HDL-C in 20 low-HDL subjects was associated with a significant reduction of plasma sICAM-1 and sE-selectin concentrations. An increased CAMs expression may be a mechanism by which a low plasma HDL level promotes atherogenesis and causes acute atherothrombotic events. PMID:11950706

Calabresi, Laura; Gomaraschi, Monica; Villa, Barbara; Omoboni, Laura; Dmitrieff, Camille; Franceschini, Guido

2002-04-01

75

Monocyte adhesion to endothelium in simian immunodeficiency virus-induced AIDS encephalitis is mediated by vascular cell adhesion molecule-1/alpha 4 beta 1 integrin interactions.  

PubMed Central

Because the mechanisms associated with recruitment of monocytes to brain in AIDS encephalitis are unknown, we used tissues from rhesus monkeys infected with simian immunodeficiency virus (SIV) to examine the relative contributions of various adhesion pathways in mediating monocyte adhesion to endothelium from encephalitic brain. Using a modified Stamper and Woodruff tissue adhesion assay, we found that the human monocytic cell lines, THP-1 and U937, and the B cell line, Ramos, preferentially bound to brain vessels from monkeys with AIDS encephalitis. Using a combined tissue adhesion/immunohistochemistry approach, these cells only bound to vessels expressing vascular cell adhesion molecule-1 (VCAM-1). Furthermore, pretreatment of tissues with antibodies to VCAM-1 or cell lines with antibodies to VLA-4 (CD49d) inhibited adhesion by more than 70%. Intercellular adhesion molecule-1 (ICAM-1)/beta 2 integrin interactions were not significant in mediating cell adhesion to the vasculature in encephalitic simian brain using a cell line (JY) capable of binding rhesus monkey ICAM-1. In addition, selectin-mediated interactions did not significantly contribute to cell binding to encephalitic brain as there was no immunohistochemical expression of E-selectin and P-selectin in either normal or encephalitic brain, nor was there a demonstrable adhesive effect from L-selectin using L-selectin-transfected 300.19 cells on simian encephalitic brain. These results demonstrate that using the tissue adhesion assay, THP-1, U937, and Ramos cells bind to vessels in brain from animals with AIDS encephalitis using VCAM-1/alpha 4 beta 1 integrin interactions and suggest that VCAM-1 and VLA-4 may be integral for monocyte recruitment to the central nervous system during the development of AIDS encephalitis. Images Figure 1

Sasseville, V. G.; Newman, W.; Brodie, S. J.; Hesterberg, P.; Pauley, D.; Ringler, D. J.

1994-01-01

76

s-ICAM-1 and s-VCAM-1 in healthy men are strongly associated with traits of the metabolic syndrome, becoming evident in the postprandial response to a lipid-rich meal  

Microsoft Academic Search

BACKGROUND: The importance of the postprandial state for the early stages of atherogenesis is increasingly acknowledged. We conducted assessment of association between postprandial triglycerides, insulin and glucose after ingestion of a standardized lipid-rich test meal, and soluble cellular adhesion molecules (sCAM) in young healthy subjects. METHODS: Metabolic parameters and sICAM-1, sVCAM-1 and E-selectin were measured before and hourly until 6

Diana Rubin; Sandra Claas; Maria Pfeuffer; Michael Nothnagel; Ulrich R Foelsch; Juergen Schrezenmeir

2008-01-01

77

Micromanipulation of adhesion of phorbol 12-myristate-13-acetate-stimulated T lymphocytes to planar membranes containing intercellular adhesion molecule-1.  

PubMed Central

This paper presents an analytical and experimental methodology to determine the physical strength of cell adhesion to a planar membrane containing one set of adhesion molecules. In particular, the T lymphocyte adhesion due to the interaction of the lymphocyte function associated molecule 1 on the surface of the cell, with its counter-receptor, intercellular adhesion molecule-1 (ICAM-1), on the planar membrane, was investigated. A micromanipulation method and mathematical analysis of cell deformation were used to determine (a) the area of conjugation between the cell and the substrate and (b) the energy that must be supplied to detach a unit area of the cell membrane from its substrate. T lymphocytes stimulated with phorbol 12-myristate-13-acetate (PMA) conjugated strongly with the planar membrane containing purified ICAM-1. The T lymphocytes attached to the planar membrane deviated occasionally from their round configuration by extending pseudopods but without changing the size of the contact area. These adherent cells were dramatically deformed and then detached when pulled away from the planar membrane by a micropipette. Detachment occurred by a gradual decrease in the radius of the contact area. The physical strength of adhesion between a PMA-stimulated T lymphocyte and a planar membrane containing 1,000 ICAM-1 molecules/micron 2 was comparable to the strength of adhesion between a cytotoxic T cell and its target cell. The comparison of the adhesive energy density, measured at constant cell shape, with the model predictions suggests that the physical strength of cell adhesion may increase significantly when the adhesion bonds in the contact area are immobilized by the actin cytoskeleton. Images FIGURE 2 FIGURE 4 FIGURE 5 FIGURE 8 FIGURE 9

Tozeren, A; Mackie, L H; Lawrence, M B; Chan, P Y; Dustin, M L; Springer, T A

1992-01-01

78

Thrombin-induced expression of endothelial P-selectin and intercellular adhesion molecule-1: a mechanism for stabilizing neutrophil adhesion  

Microsoft Academic Search

Thrombin-induced expression of endothelial adhesivity toward neutrophils (PMN) was studied using human umbilical vein endothelial cells (HUVEC). HUVEC were challenged with human ot-thrombin for varying durations up to 120 min, after which the cells were fixed with 1% paraformaldehyde and 5~Cr-labeled human PMN were added to determine PMN adhesion. Endothelial adhesivity increased within 15 min after c~-thrombin exposure, and the

Yasuo Sugama; Chinnaswamy Tiruppathi; Kilambi Janakidevi; Thomas T. Andersen; John W. Fenton II; Asrar B. Malik

1992-01-01

79

Induction of intercellular adhesion molecule-1 in human nasal epithelial cells during respiratory syncytial virus infection.  

PubMed Central

The effects of infection with respiratory syncytial virus (RSV) on expression of intercellular adhesion molecule (ICAM)-1 was determined in vitro in nasal epithelial cell cultures. Functional consequences of changes in ICAM-1 expression were assessed by measuring adhesion of a human leukaemic T-cell line to RSV-infected epithelial cells. Also, adhesion of phytohaemagglutinin-activated tonsillar lymphocytes (TL) to RSV-infected epithelial cells caused a significant increase in interleukin (IL)-4 or IL-5 production. Release of these cytokines was adhesion dependent as non-adherent TL produced significantly less IL-4 or IL-5. However, no significant difference was observed for IL-2 or interferon-gamma (IFN-gamma) production. These observations suggest that RSV-infected epithelial cells may induce T-helper type-2 (Th2)-like cytokines by mucosal lymphocytes during mucosal infection in vivo. Images Figure 1 Figure 2

Matsuzaki, Z; Okamoto, Y; Sarashina, N; Ito, E; Togawa, K; Saito, I

1996-01-01

80

Vascular Cell Adhesion Molecule-1 Expression and Signaling During Disease: Regulation by Reactive Oxygen Species and Antioxidants  

PubMed Central

Abstract The endothelium is immunoregulatory in that inhibiting the function of vascular adhesion molecules blocks leukocyte recruitment and thus tissue inflammation. The function of endothelial cells during leukocyte recruitment is regulated by reactive oxygen species (ROS) and antioxidants. In inflammatory sites and lymph nodes, the endothelium is stimulated to express adhesion molecules that mediate leukocyte binding. Upon leukocyte binding, these adhesion molecules activate endothelial cell signal transduction that then alters endothelial cell shape for the opening of passageways through which leukocytes can migrate. If the stimulation of this opening is blocked, inflammation is blocked. In this review, we focus on the endothelial cell adhesion molecule, vascular cell adhesion molecule-1 (VCAM-1). Expression of VCAM-1 is induced on endothelial cells during inflammatory diseases by several mediators, including ROS. Then, VCAM-1 on the endothelium functions as both a scaffold for leukocyte migration and a trigger of endothelial signaling through NADPH oxidase-generated ROS. These ROS induce signals for the opening of intercellular passageways through which leukocytes migrate. In several inflammatory diseases, inflammation is blocked by inhibition of leukocyte binding to VCAM-1 or by inhibition of VCAM-1 signal transduction. VCAM-1 signal transduction and VCAM-1-dependent inflammation are blocked by antioxidants. Thus, VCAM-1 signaling is a target for intervention by pharmacological agents and by antioxidants during inflammatory diseases. This review discusses ROS and antioxidant functions during activation of VCAM-1 expression and VCAM-1 signaling in inflammatory diseases. Antioxid. Redox Signal. 15, 1607–1638.

Marchese, Michelle E.; Abdala-Valencia, Hiam

2011-01-01

81

Selective inhibition by alpha-tocopherol of vascular cell adhesion molecule-1 expression in human vascular endothelial cells.  

PubMed

An early event in atherogenesis is the adhesion of monocytes to endothelium via adhesion molecules such as VCAM-1 and intracellular adhesion molecule-1 (ICAM-1). It has been suggested that VCAM-1 plays a very important role in recruitment of monocytes in atherosclerosis. Several studies suggest that vitamin E has antiatherosclerotic properties. However, the mechanism of its antiatherogenic effect awaits elucidation. The aim of our study was to evaluate whether alpha-tocopherol can influence expression of endothelial cell adhesion molecules and endothelial adhesiveness. The study was performed on cultured human umbilical vein endothelial cells (HUVEC). HUVEC were pretreated with alpha-tocopherol (50 micromol/l) in different times before stimulation with TNFalpha (100 U/ml) or IL-1beta (100 U/ml). Protein expression of VCAM-1 and ICAM-1 was measured by flow cytometry. mRNA expression of VCAM-1 was measured by reverse transcription polymerase chain reaction (RT-PCR). alpha-Tocopherol time dependently reduced agonist-induced VCAM-1 in both surface protein (about 40%, 48 h) and mRNA (about 35%, 48 h) expression in HUVEC but not ICAM-1 surface protein expression. Inhibitory effect of alpha-tocopherol was dependent on culture condition of HUVEC. Decreased VCAM-1 expression was associated with reduction (about 40%) of adherence between cytokine-stimulated HUVEC and peripheral blood mononuclear leukocytes (PBMC). Our results suggest that the antiatherogenic effect of alpha-tocopherol may in part be due to a downregulation of VCAM-1 expression. PMID:10924325

Zapolska-Downar, D; Zapolski-Downar, A; Markiewski, M; Ciechanowicz, A; Kaczmarczyk, M; Naruszewicz, M

2000-08-11

82

Selective inhibition by probucol of vascular cell adhesion molecule-1 (VCAM-1) expression in human vascular endothelial cells.  

PubMed

An early event in atherogenesis is the adhesion of monocytes to endothelium via adhesion molecules, such as VCAM-1 and intracellular adhesion molecule-1 (ICAM-1). It has been suggested that VCAM-1 plays a very important role in the recruitment of monocytes in atherosclerosis. Probucol is a potent inhibitor of atherosclerosis in animal models. However, the mechanism of its antiatherogenic effect is poorly understood. The aim of our study was to evaluate whether probucol can influence the expression of endothelial cell adhesion molecules and endothelial adhesiveness. The study was performed on cultured human umbilical vein endothelial cells (HUVEC). HUVEC were pretreated with probucol (50 microM) at different time periods before stimulation with TNFalpha (100 U ml(-1)) or IL-1beta (100 U ml(-1)). The protein expression of VCAM-1 and ICAM-1 was measured by flow cytometry. VCAM-1 mRNA expression was measured by reverse transcription polymerase chain reaction (RT PCR). Probucol time dependently reduced agonist-induced VCAM-1 ( approximately 45%, 48 h) surface protein and mRNA expression ( approximately 40%, 48 h) in HUVEC, but not ICAM-1 surface protein expression. Decreased VCAM-1 expression was associated with reduction ( approximately 40%) of adherence between cytokine-stimulated HUVEC and peripheral blood mononuclear leukocytes (PBMC). Our results suggest that the antiatherogenic effect of probucol may, in part, be due to a downregulation of VCAM-1 expression. PMID:11223433

Zapolska-Downar, D; Zapolski-Downar, A; Markiewski, M; Ciechanowicz, A; Kaczmarczyk, M; Naruszewicz, M

2001-03-01

83

Human Dermal Mast Cells Contain and Release Tumor Necrosis Factor ?, which Induces Endothelial Leukocyte Adhesion Molecule 1  

NASA Astrophysics Data System (ADS)

Tumor necrosis factor ? (TNF-?) is a proinflammatory cytokine that mediates endothelial leukocyte interactions by inducing expression of adhesion molecules. In this report, we demonstrate that human dermal mast cells contain sizeable stores of immunoreactive and biologically active TNF-? within granules, which can be released rapidly into the extracellular space upon degranulation. Among normal human dermal cells, mast cells are the predominant cell type that expresses both TNF-? protein and TNF-? mRNA. Moreover, induction of endothelial leukocyte adhesion molecule 1 expression is a direct consequence of release of mast cell-derived TNF-?. These findings establish a role for human mast cells as "gatekeepers" of the dermal microvasculature and indicate that mast cell products other than vasoactive amines influence endothelium in a proinflammatory fashion.

Walsh, Laurence J.; Trinchieri, Giorgio; Waldorf, Heidi A.; Whitaker, Diana; Murphy, George F.

1991-05-01

84

Nitric Oxide Pretreatment Enhances Atheroma Component Highlighting in Vivo with Intercellular Adhesion Molecule-1-Targeted Echogenic Liposomes.  

PubMed

We present an ultrasound technique for the detection of inflammatory changes in developing atheromas. We used contrast-enhanced ultrasound imaging with (i) microbubbles targeted to intercellular adhesion molecule-1 (ICAM-1), a molecule of adhesion involved in inflammatory processes in lesions of atheromas in New Zealand White rabbits, and (ii) pretreatment with nitric oxide-loaded microbubbles and ultrasound activation at the site of the endothelium to enhance the permeability of the arterial wall and the penetration of ICAM-1-targeted microbubbles. This procedure increases acoustic enhancement 1.2-fold. Pretreatment with nitric oxide-loaded echogenic liposomes and ultrasound activation can potentially facilitate the subsequent penetration of targeted echogenic liposomes into the arterial wall, thus allowing improved detection of inflammatory changes in developing atheromas. PMID:24613216

Kee, Patrick H; Kim, Hyunggun; Huang, Shaoling; Laing, Susan T; Moody, Melanie R; Vela, Deborah; Klegerman, Melvin E; McPherson, David D

2014-06-01

85

Chemistry on a Single Protein, Vascular Cell Adhesion Molecule1, during Forced Unfolding  

Microsoft Academic Search

Proteins of many types experience tensile forces in their normal function, and vascular cell adhesion mole- cule-1 (VCAM-1) is typical in this. VCAM has seven Ig domains, and each has a disulfide bond (-S-S-) buried in its core that covalently stabilizes about half of each domain against unfolding. VCAM is extended here by single molecule atomic force microscopy in the

Nishant Bhasin; Philippe Carl; Sandy Harper; Gang Feng; Hui Lu; David W. Speicher

2004-01-01

86

Soluble endothelium-associated adhesion molecules in patients with Graves' disease.  

PubMed

The targeting and recruitment of inflammatory cells to vascular endothelium in Graves' disease (GD) is mediated by intercellular adhesion molecule-1 (ICAM-1), endothelial leucocyte adhesion molecule-1 (ELAM-1), and vascular cell adhesion molecule-1 (VCAM-1). We have studied serum levels of soluble ICAM-1 (sICAM-1), soluble ELAM-1 (sELAM-1), and soluble VCAM-1 (sVCAM-1) in patients with GD (n = 21) and in patients with iodine-deficient goitre (IDG) (n = 23). The serum levels of sICAM-1 were markedly elevated in patients with GD before treatment with thiamazole (median 560 ng/ml versus 185 ng/ml in patients with IDG). In addition, elevated serum concentrations of sELAM-1 (median 85 ng/ml versus 33 ng/ml, respectively) and sVCAM-1 (median 42 ng/ml versus 15 ng/ml, respectively) were observed in patients with GD (P < 0.01 for all). The serum levels of sELAM-1 and sVCAM-1 dropped significantly after initiation of therapy and were within the normal range after 4, and 8 weeks of therapy, respectively. Serum levels of sICAM-1 were elevated even after 8 weeks of therapy. Serum levels of sVACM-1 and sICAM-1 correlated with the serum concentrations of anti-thyroid-stimulating hormone (TSH)-receptor antibodies (TSHR-R) (n = 21; r = 0.929 and r = 0.810, respectively) and anti-thyroid peroxidase antibodies (TPO-Ab) (n = 21; r = 0.673 and r = 0.750, respectively). However, no correlation between sELAM-1 and TPO-Ab, TSHR-R, and anti-thyroglobulin antibodies (Tg-Ab), respectively, could be found. In addition to thyroid hormones and autoantibodies, serum concentrations of sELAM-1 and sVCAM-1, but not sICAM-1, could be useful as clinical markers for disease activity. PMID:7525128

Wenisch, C; Myskiw, D; Parschalk, B; Hartmann, T; Dam, K; Graninger, W

1994-11-01

87

Soluble endothelium-associated adhesion molecules in patients with Graves' disease.  

PubMed Central

The targeting and recruitment of inflammatory cells to vascular endothelium in Graves' disease (GD) is mediated by intercellular adhesion molecule-1 (ICAM-1), endothelial leucocyte adhesion molecule-1 (ELAM-1), and vascular cell adhesion molecule-1 (VCAM-1). We have studied serum levels of soluble ICAM-1 (sICAM-1), soluble ELAM-1 (sELAM-1), and soluble VCAM-1 (sVCAM-1) in patients with GD (n = 21) and in patients with iodine-deficient goitre (IDG) (n = 23). The serum levels of sICAM-1 were markedly elevated in patients with GD before treatment with thiamazole (median 560 ng/ml versus 185 ng/ml in patients with IDG). In addition, elevated serum concentrations of sELAM-1 (median 85 ng/ml versus 33 ng/ml, respectively) and sVCAM-1 (median 42 ng/ml versus 15 ng/ml, respectively) were observed in patients with GD (P < 0.01 for all). The serum levels of sELAM-1 and sVCAM-1 dropped significantly after initiation of therapy and were within the normal range after 4, and 8 weeks of therapy, respectively. Serum levels of sICAM-1 were elevated even after 8 weeks of therapy. Serum levels of sVACM-1 and sICAM-1 correlated with the serum concentrations of anti-thyroid-stimulating hormone (TSH)-receptor antibodies (TSHR-R) (n = 21; r = 0.929 and r = 0.810, respectively) and anti-thyroid peroxidase antibodies (TPO-Ab) (n = 21; r = 0.673 and r = 0.750, respectively). However, no correlation between sELAM-1 and TPO-Ab, TSHR-R, and anti-thyroglobulin antibodies (Tg-Ab), respectively, could be found. In addition to thyroid hormones and autoantibodies, serum concentrations of sELAM-1 and sVCAM-1, but not sICAM-1, could be useful as clinical markers for disease activity.

Wenisch, C; Myskiw, D; Parschalk, B; Hartmann, T; Dam, K; Graninger, W

1994-01-01

88

Lactosylceramide Mediates Shear-Induced Endothelial Superoxide Production and Intercellular Adhesion Molecule1 Expression  

Microsoft Academic Search

Laminar shear stress activates NADPH oxidase in vascular endothelial cells (ECs), and the generated superoxide radicals (O2–·) are known to be involved in intercellular adhesion molecule (ICAM)-1 expression. In this study, the role of a glycosphingolipid (GSL), lactosylceramide (LacCer), as a second messenger in the shear-induced O2–· generation and ICAM-1 expression was examined. It is known that glucosylceramide synthase (GlcT-1)

Li-Hong Yeh; Adam M. Kinsey; Subroto Chatterjee; B. Rita Alevriadou

2001-01-01

89

Benzo[a]pyrene induces intercellular adhesion molecule-1 through a caveolae and aryl hydrocarbon receptor mediated pathway  

PubMed Central

Toxicologic and epidemiologic studies have linked benzo[a]pyrene (B[a]P) exposure with cardiovascular diseases such as atherosclerosis. The mechanisms of action leading to these diseases have not been fully understood. One key step in the development of atherosclerosis is vascular endothelial dysfunction, which is characterized by increased adhesiveness. To determine if B[a]P could lead to increased endothelial adhesiveness, the effects of B[a]P on human endothelial cell intercellular adhesion molecule-1 (ICAM-1) expression was investigated. B[a]P was able to increase ICAM-1 protein only after pretreatment with the aryl hydrocarbon receptor (AhR) agonist ?-naphthoflavone (?-NF). Knockdown of AhR by siRNA or treatment with AhR antagonist ?-naphthoflavone (?-NF) eliminated the induction of ICAM-1 from B[a]P, confirming the necessity of AhR in this process. Likewise, B[a]P only increased monocyte adhesion to the vascular endothelium when cells were pretreated with ?-NF. Experiments were done to define a signaling mechanism. B[a]P increased phosphorylation of MEK and p38-MAPK, and inhibitors to these proteins blunted the ICAM-1 induction. B[a]P was also able to increase AP-1 DNA binding and phosphorylation of c-Jun. Phosphorylation of c-Jun was disrupted by MEK and p38-MAPK inhibitors linking the signaling cascade. Finally, the importance of membrane microdomains, caveolae, was demonstrated by knockdown of the structural protein caveolin-1. Disruption of caveolae eliminated the B[a]P induced ICAM-1 expression. These data suggest a possible pro-inflammatory mechanism of action of B[a]P involving caveolae, leading to increased vascular endothelial adhesiveness, and this inflammation may be a critical step in the development of B[a]P-induced atherosclerosis.

Oesterling, Elizabeth; Toborek, Michal; Hennig, Bernhard

2008-01-01

90

Intercellular adhesion molecule 1 (ICAM-1) has a central role in cell-cell contact-mediated immune mechanisms.  

PubMed Central

The role of intercellular adhesion molecule 1 (ICAM-1) in immune function was probed by using the Wehi-CAM-1 (W-CAM-1) monoclonal antibody. This antibody blocks aggregation of cell lines mediated by the ICAM-1 molecule and is here shown to block homotypic binding of purified populations of activated T and B lymphocytes (blasts) and also aggregation of mixed T- and B-cell blasts. We also demonstrate that W-CAM-1 inhibited T-cell adhesion to normal human endothelial cells, the first step in lymphocyte egress into the tissues. In tests of immune function, W-CAM-1 had a modest inhibitory effect on T- and B-cell activation by potent mitogens and no effect on the response of activated lymphocytes to lymphokines. By contrast, activation induced by cell-cell contact (mixed lymphocyte reaction, T-cell-mediated B-cell activation) was significantly inhibited. Moreover, the antibody was shown to block elements of both effector arms of the immune system (cytotoxic cell function and immunoglobulin production). These findings show that the ICAM-1 molecule is a central component of the mechanism of lymphocyte-endothelial cell adhesion. The studies of lymphoid function demonstrate a pivotal role for this molecule in both the T-cell/T-cell and T-cell/B-cell interactions, which underpin the regulation of the immune response, and in the mechanism of cell-mediated cytotoxicity.

Boyd, A W; Wawryk, S O; Burns, G F; Fecondo, J V

1988-01-01

91

Epidermal Expression of Intercellular Adhesion Molecule 1 is Not a Primary Inducer of Cutaneous Inflammation in Transgenic Mice  

NASA Astrophysics Data System (ADS)

Keratinocytes at sites of cutaneous inflammation have increased expression of intercellular adhesion molecule 1 (ICAM-1), a cytokine-inducible adhesion molecule which binds the leukocyte integrins LFA-1 and Mac-1. Transgenic mice were prepared in which the expression of mouse ICAM-1 was targeted to basal keratinocytes by using the human K14 keratin promoter. The level of constitutive expression attained in the transgenic mice exceeded the peak level of ICAM-1 expression induced on nontransgenic mouse keratinocytes in vitro by optimal combinations of interferon ? and tumor necrosis factor ? or in vivo by proinflammatory stimuli such as phorbol 12-myristate 13-acetate. In vitro adhesion assays demonstrated that cultured transgenic keratinocytes were superior to normal keratinocytes as a substrate for the LFA-1-dependent binding of mouse T cells, confirming that the transgene-encoded ICAM-1 was expressed in a functional form. However, the high level of constitutive ICAM-1 expression achieved on keratinocytes in vivo in these transgenic mice did not result in additional recruitment of CD45^+ leukocytes into transgenic epidermis, nor did it elicit dermal inflammation. Keratinocyte ICAM-1 expression also did not potentiate contact-hypersensitivity reactions to epicutaneous application of haptens. The absence of a spontaneous phenotype in these transgenic mice was not the result of increased levels of soluble ICAM-1, since serum levels of soluble ICAM-1 were equal in transgenic mice and controls. We conclude that elevated ICAM-1 expression on keratinocytes cannot act independently to influence leukocyte trafficking and elicit cutaneous inflammation.

Williams, Ifor R.; Kupper, Thomas S.

1994-10-01

92

Changes in the vascular cell adhesion molecule-1, intercellular adhesion molecule-1 and c-reactive protein following administration of aqueous extract of piper sarmentosum on experimental rabbits fed with cholesterol diet  

PubMed Central

Background Inflammation process plays an important role in the development of atherosclerosis. Hypercholesterolemia is one of the major risk factors for atherosclerosis. The present study aimed to evaluate the effect of aqueous extract of Piper sarmentosum (P.s) on inflammatory markers like vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and C-reactive protein (CRP). Methods Forty two male New Zealand white rabbits were divided equally into seven groups; (i) C- control group fed normal rabbit chow (ii) CH- cholesterol diet (1%cholesterol) (iii) X1- 1% cholesterol with water extract of P.s (62.5 mg/kg) (iv) X2- 1% cholesterol with water extract of P.s (125 mg/kg (v) X3- 1% cholesterol with water extract of P.s (250 mg/kg) (vi) X4- 1% cholesterol with water extract of P.s (500 mg/kg) and (vii) SMV group fed with 1% cholesterol supplemented with simvistatin drug (1.2 mg/kg). All animals were treated for 10 weeks. Blood serum was taken for observing the inflammatory markers at the beginning and end of the experiment. Results Rabbits fed with 1% cholesterol diet (CH) showed significant increase in the level of VCAM-1, ICAM-1 and CRP compared to the C group. The levels of VCAM-1, ICAM-1 and CRP in the 1% cholesterol group and supplemented with P.s (500 mg/kg) were significantly reduced compared to the cholesterol group. Similar results were also reported with simvistatin group. Conclusion These results suggest that the supplementation of Piper sarmentosum extract could inhibit inflammatory markers which in turn could prevent atherosclerosis.

2011-01-01

93

Intercellular adhesion molecule-1, intercellular adhesion molecule-3, and leukocyte integrins in leukocyte accumulation in membranoproliferative glomerulonephritis type i  

Microsoft Academic Search

Marked intraglomerular infiltration of leukocytes is observed in membranoproliferative glomerulonephritis (MPGN). We recently demonstrated that this leukocyte infiltration develops partly through macrophage-1 (Mac1)-positive cells and glomerular C3c deposits (Clin Exp Immunol 100:269–276, 1995). To further investigate the mediation of adhesion molecules in the leukocyte accumulation, we immunohistochemically examined the expression of intraglomerular leukocyte integrins and their ligands as well as

Jun Soma; Takao Saito; Tetsuya Ootaka; Hiroshi Sato; Keishi Abe

1996-01-01

94

Platelet-endothelial cell adhesion molecule-1 gene polymorphism and its soluble level are associated with ischemic stroke.  

PubMed

Inflammation, characterized by the recruitment and adhesion of circulating leukocytes by cellular adhesion molecules, plays an important role in the pathogenesis of atherosclerosis. Genetic analyses of platelet-endothelial cell adhesion molecule-1 (PECAM-1), a key adhesion molecule in the progression of atherosclerosis, have provided conflicting results regarding the role of variation within the PECAM-1 gene and risk for coronary heart disease. No studies have examined the association of this polymorphism with ischemic stroke. Therefore, we investigated that PECAM-1 gene polymorphism and its soluble level are associated with ischemic stroke in Chinese population. We analyzed single-nucleotide polymorphisms of PECAM-1 gene Leu125Val, Asn563Ser, and Gly670Arg in 265 patients with ischemic stroke and 280 age- and sex-matched controls, using polymerase chain reaction-restriction fragment length polymorphism and DNA sequencing method, while soluble PECAM-1 (sPECAM-1) levels were measured by enzyme-linked immunosorbent assay. There were significant differences in the genotype and allele frequencies of PECAM-1 gene Leu125Val polymorphism between the group of patients with ischemic stroke and the control group (p < 0.05). sPECAM-1 levels were increased in patients with ischemic stroke compared with controls (p < 0.01). Moreover, genotypes carrying the PECAM-1 125Val variant allele were associated with increased PECAM-1 levels compared to the homozygous wild-type genotype in patients with ischemic stroke. The Leu125Val polymorphism of PECAM-1 and its sPECAM-1 levels are associated with ischemic stroke in Chinese population. Our data suggest that the PECAM-1 gene may play a role in the development of ischemic stroke. PMID:19183069

Wei, Ye-Sheng; Lan, Yan; Liu, Yun-Guang; Meng, Lan-Qing; Xu, Qun-Qing; Xie, Hai-Yuan

2009-03-01

95

Enhanced expression of intracellular adhesion molecule-1 and P-selectin in the diabetic human retina and choroid.  

PubMed Central

Elevated expression of intercellular adhesion molecule-1 (ICAM-1) as well as E- and P-selectin occurs on the vascular endothelium in a number of disease states and is thought to play an early critical role in the adhesion of circulating leukocytes to the endothelium. The goal of the present study was to investigate the immunolocalization of these molecules in the retina and choroid of postmortem human tissue sections from nondiabetic and diabetic subjects. Whereas ICAM-1 was localized primarily within the choriocapillaris of nondiabetic subjects, immunoreactivity in diabetics was significantly elevated throughout the choroidal vasculature and within retinal blood vessels (P < 0.05). In the choroid, P-selectin was most prominent in veins of the nondiabetic, whereas in diabetics, P-selectin was significantly elevated in arteries (P < 0.001) and veins (P < 0.05) and, in some cases, was also observed in choriocapillaris. P-selectin immunoreactivity was not observed in the retina of any subject. E-selectin immunoreactivity was not observed in choroid or retina in any subjects. Neutrophil numbers per square millimeter of tissue were significantly elevated in diabetic choroid (P < 0.05) and retina (P < 0.001). Our results demonstrate that ICAM-1 and P-selectin are constitutively expressed in the normal choroid and are upregulated in the choroidal vasculature in diabetes, but only ICAM-1 was upregulated in the retina of diabetic subjects. Increased cell adhesion molecule expression may contribute to the retinal and choroidal microangiopathy observed in diabetics by enhancing leukocyte adhesion and consequently the incidence of capillary obstruction and endothelial cell injury. Images Figure 1 Figure 2 Figure 3 Figure 4

McLeod, D. S.; Lefer, D. J.; Merges, C.; Lutty, G. A.

1995-01-01

96

Organization, regulatory sequences, and alternatively spliced transcripts of the mucosal addressin cell adhesion molecule-1 (MAdCAM-1) gene  

SciTech Connect

The mucosal addressin cell adhesion molecule-1 (MAdCAM-1) is expressed selectively at venular sites of lymphocyte extravasation into mucosal lymphoid tissues and lamina propria, where it directs local lymphocyte trafficking. MAdCAM-1 is a multifunctional type I transmembrane adhesion molecule comprising two distal Ig domains involved in {alpha}4{beta}7 integrin binding, a mucin-like region able to display L-selectin-binding carbohydrates, and a membrane-proximal Ig domain homologous to IgA. We show in this work that the MAdCAM-1 gene is located on chromosome 10 and contains five exons. The signal peptide and each one of the three Ig domains are encoded by a distinct exon, whereas the transmembrane, cytoplasmic tail, and 3{prime}-untranslated region of MAdCAM-1 are combined on a single exon. The mucin-like region and the third Ig domain are encoded together on exon 4. An alternatively spliced MAdCAM-1 mRNA is identified that lacks the mucin/IgA-homologous exon 4-encoded sequences. This short variant of MAdCAM-1 may be specialized to support {alpha}4{beta}7-dependent adhesion strengthening, independent of carbohydrate-presenting function. Sequences 5{prime} of the transcription start site include tandem nuclear factor-KB sites; AP-1, AP-2, and signal peptide-1 binding sites; and an estrogen response element. Our findings reinforce the correspondence between the multidomain structure and versatile functions of this vascular addressin, and suggest an additional level of regulation of carbohydrate-presenting capability, and thus of its importance in lectin-mediated vs. {alpha}4{beta}7-dependent adhesive events in lymphocyte trafficking. 46 refs., 6 figs., 1 tab.

Sampaio, S.O.; Mei, C.; Butcher, E.C. [Stanford Univ. School of Medicine, CA (United States)] [and others

1995-09-01

97

Role of E-selectin and platelet endothelial cell adhesion molecule 1 in gastritis in food allergy patients  

PubMed Central

Introduction The prevalence of food allergies and other allergic reactions is increasing worldwide, particularly in highly-urbanized populations. Cell adhesion molecules are expressed in response to various pro-inflammatory cytokines. The expression of intercellular adhesion molecule 1 – ICAM-1 (CD54), ICAM-1 (CD106), P-selectin (CD62P), and E-selectin (CD62E) on vascular endothelial cells is induced by such pro-inflammatory cytokines as tumor necrosis factor ? (TNF-?) and interleukin-1 (IL-1). Aim To analyze concentrations of E-selectin and platelet endothelial cell adhesion molecule-1 (PECAM-1) in patients with an allergic type of food sensitivity co-existing with gastritis and to compare them to the values determined in individuals with dyspeptic symptoms not associated with allergic disorders. Material and methods The study included 80 patients, among them 50 individuals with food sensitivity confirmed based on compulsory standards, and 30 subjects with dyspeptic symptoms not accompanied by allergic conditions. Venous blood samples were taken from each patient and concentrations of E-selectin and PECAM-1 were determined by means of ELISA. Results Mean concentrations of sE-selectin and sPECAM-1 in patients with food allergy amounted to 54.0 ±21.6 ng/ml and 132.8 ±31.4 ng/ml, respectively. In individuals without food allergy, mean concentrations of sE-selectin and sPECAM-1 were 57.7 ±17.9 ng/ml and 139.6 ±31.1 ng/ml, respectively. Patients with food allergy and individuals with dyspeptic symptoms not associated with food allergy did not differ significantly in terms of sE-selectin concentrations (Mann-Whitney U-test, p = 0.453028). Similarly, no significant intergroup differences were observed with regard to sPECAM-1 concentrations (Mann-Whitney U-test, p = 0.231054). Conclusions Adhesion molecules play an important role in the development of inflammation. This study did not find significant differences in the concentrations of such molecules as sE-selectin and sPECAM-1 between patients with food allergy and gastritis, and subjects in whom gastritis was not accompanied by atopic disorders. A positive correlation between the concentrations of sPECAM-1 and E-selectin was observed in food allergy patients. Consequently, it can be concluded that these molecules participate in the pathogenesis of the inflammatory process independently of the etiopathogenesis of gastritis.

Przybyszewski, Michal; Kuzminski, Andrzej; Tlappa, Jacek; Mucka, Jacek; Napiorkowska, Katarzyna; Szynkiewicz, Ewa; Zbikowska-Gotz, Magdalena; Bartuzi, Zbigniew

2013-01-01

98

Involvement of Intercellular Adhesion Molecule-1 Up-Regulation in Bradykinin Promotes Cell Motility in Human Prostate Cancers  

PubMed Central

Prostate cancer is the most commonly diagnosed malignancy in men and shows a predilection for metastasis to distant organs. Bradykinin (BK) is an inflammatory mediator and has recently been shown to mediate tumor growth and metastasis. The adhesion molecule intercellular adhesion molecule-1 (ICAM-1) plays a critical role during tumor metastasis. The aim of this study was to examine whether BK promotes prostate cancer cell migration via ICAM-1 expression. The motility of cancer cells was increased following BK treatment. Stimulation of prostate cancer cells with BK induced mRNA and protein expression of ICAM-1. Transfection of cells with ICAM-1 small interfering RNA reduced BK-increased cell migration. Pretreatment of prostate cancer cells with B2 receptor, phosphatidylinositol 3-kinase (PI3K), Akt, and activator protein 1 (AP-1) inhibitors or mutants abolished BK-promoted migration and ICAM-1 expression. In addition, treatment with a B2 receptor, PI3K, or Akt inhibitor also reduced BK-mediated AP-1 activation. Our results indicate that BK enhances the migration of prostate cancer cells by increasing ICAM-1 expression through a signal transduction pathway that involves the B2 receptor, PI3K, Akt, and AP-1. Thus, BK represents a promising new target for treating prostate cancer metastasis.

Yu, Hsin-Shan; Lin, Tien-Huang; Tang, Chih-Hsin

2013-01-01

99

Expression of CD31/PECAM-1 (Platelet Endothelial Cell Adhesion Molecule 1) by Blastic Plasmacytoid Dendritic Cell Neoplasms  

PubMed Central

IMPORTANCE Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare malignant neoplasm with cutaneous manifestations and a rapidly progressive clinical course. The diagnosis relies on characteristic clinicopathologic and immunopathologic features. However, the overlap of immunophenotypic features with other cancers, as well as newly discovered interpersonal and intrapersonal phenotypic variations, renders the identification of BPDCN challenging. A greater understanding of the proteins expressed by BPDCN might facilitate its recognition and provide insights into its clinical behavior. OBSERVATIONS In 7 of 9 patients at 4 tertiary care institutions, immunohistochemical analysis demonstrated strong CD31/PECAM-1 (platelet endothelial cell adhesion molecule 1) expression by neoplastic cells. Combined with similar findings observed in 1 former patient, 8 of 10 cases of BPDCN were CD31/PECAM-1 positive. CONCLUSIONS AND RELEVANCE Expression of CD31/PECAM-1 by BPDCN adds new information about the antigenic profile of this unusual neoplasm. CD31/PECAM-1 influences multiple cell functions including adhesion, apoptosis, coagulation, host response, and protein synthesis that might affect clinical features of BPDCN such as hemorrhage, aggressive tumor growth, and resistance to therapy. Therefore, the potential role of this molecule in the tumor formation and progression of BPDCN warrants additional exploration.

Salva, Katrin A.; Haemel, Anna K.; Pincus, Laura B.; Liu, Jing; Sundram, Uma; Guitart, Joan; Longley, B. Jack; Wood, Gary S.

2014-01-01

100

The integrin alpha9beta1 mediates adhesion to activated endothelial cells and transendothelial neutrophil migration through interaction with vascular cell adhesion molecule-1.  

PubMed

The integrin alpha9beta1 has been shown to be widely expressed on smooth muscle and epithelial cells, and to mediate adhesion to the extracellular matrix proteins osteopontin and tenascin-C. We have found that the peptide sequence this integrin recognizes in tenascin-C is highly homologous to the sequence recognized by the closely related integrin alpha4beta1, in the inducible endothelial ligand, vascular cell adhesion mole-cule-1 (VCAM-1). We therefore sought to determine whether alpha9beta1 also recognizes VCAM-1, and whether any such interaction would be biologically significant. In this report, we demonstrate that alpha9beta1 mediates stable cell adhesion to recombinant VCAM-1 and to VCAM-1 induced on human umbilical vein endothelial cells by tumor necrosis factor-alpha. Furthermore, we show that alpha9beta1 is highly and selectively expressed on neutrophils and is critical for neutrophil migration on VCAM-1 and tenascin-C. Finally, alpha9beta1 and alpha4 integrins contribute to neutrophil chemotaxis across activated endothelial monolayers. These observations suggest a possible role for alpha9beta1/VCAM-1 interactions in extravasation of neutrophils at sites of acute inflammation. PMID:10209034

Taooka, Y; Chen, J; Yednock, T; Sheppard, D

1999-04-19

101

The Role of Platelet\\/Endothelial Cell Adhesion Molecule1 (CD31) and CD38 Antigens in Marrow Microenvironmental Retention of Acute Myelogenous Leukemia Cells  

Microsoft Academic Search

In acute myelogenous leukemia (AML), leukemic cell-micro- environment interactions within various niches (stromal\\/ osteoblastic or sinusoidal endothelial cell niches) have a role in leukemia cell survival and drug resistance. The AML leukemic cells express platelet\\/endothelial cell adhesion molecule-1 (CD31) and CD38, two adhesion molecules that could interact with microenvironmental elements, i.e., CD31 on the surface of marrow endothelial cells (CD31\\/CD31

Nathalie Gallay; Ludovic Anani; Adriana Lopez; Philippe Colombat; Christian Binet; Jorge Domenech; Babette B. Weksler; Fabio Malavasi; UniversiteFrancois Rabelais

102

Induction of Intercellular Adhesion Molecule1 on Human Brain Endothelial Cells by HIV1 gp120: Role of CD4 and Chemokine Coreceptors  

Microsoft Academic Search

Central nervous system dysfunction is commonly observed in children with HIV-1 infection, but the mechanisms whereby HIV-1 causes encephalopathy are not completely understood. We have previously shown that human brain microvascular endothelial cells (HBMEC) from children are responsive to gp120 derived from X4 HIV-1 by increasing expression of intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule-1. However, the mechanisms

Monique F. Stins; Donna Pearce; Francescopaolo Di Cello; Anat Erdreich-Epstein; Carlos A Pardo; Kwang Sik Kim

2003-01-01

103

Cytokine-induced upregulation of hepatic intercellular adhesion molecule-1 messenger RNA expression and its role in the pathophysiology of murine endotoxin shock and acute liver failure  

Microsoft Academic Search

Neutrophil-induced liver injury during endotoxemia is dependent on the adhesion molecule Mac-1 (CD11b\\/CD18) on neutrophils. The potential involvement of its counterreceptor, intercellular adhesion molecule1 (ICAM-1), in the pathogenesis was investigated after administration of 100 ?g\\/kg Salmonella abortus equi endotoxin (ET) in galactosamine-sensitized mice (Gal). In ETsensitive mice (C3Heb\\/FeJ), which generated large amounts of tumor necrosis factor—alpha (TNF-?), massive neutrophil infiltration

Naeem A. Essani; Michael A. Fisher; Anwar Farhood; Anthony M. Manning; C. Wayne Smith; Hartmut Jaeschke

1995-01-01

104

Ambient pollutants, polymorphisms associated with microRNA processing and adhesion molecules: the Normative Aging Study  

PubMed Central

Background Particulate air pollution has been associated with cardiovascular morbidity and mortality, but it remains unclear which time windows and pollutant sources are most critical. MicroRNA (miRNA) is thought to be involved in cardiovascular regulation. However, little is known about whether polymorphisms in genes that process microRNAs influence response to pollutant exposure. We hypothesized that averaging times longer than routinely measured one or two day moving averages are associated with higher soluble intercellular adhesion molecule-1 (sICAM-1) and vascular cell adhesion molecule-1 (sVCAM-1) levels, and that stationary and mobile sources contribute differently to these effects. We also investigated whether single nucleotide polymorphisms (SNPs) in miRNA-processing genes modify these associations. Methods sICAM-1 and sVCAM-1 were measured from 1999-2008 and matched to air pollution monitoring for fine particulate matter (PM2.5) black carbon, and sulfates (SO42-). We selected 17 SNPs in five miRNA-processing genes. Mixed-effects models were used to assess effects of pollutants, SNPs, and interactions under recessive inheritance models using repeated measures. Results 723 participants with 1652 observations and 1-5 visits were included in our analyses for black carbon and PM2.5. Sulfate data was available for 672 participants with 1390 observations. An interquartile range change in seven day moving average of PM2.5 (4.27 ?g/m3) was associated with 3.1% (95%CI: 1.6, 4.6) and 2.5% (95%CI: 0.6, 4.5) higher sICAM-1 and sVCAM-1. Interquartile range changes in sulfates (1.39 ?g/m3) were associated with 1.4% higher (95%CI: 0.04, 2.7) and 1.6% (95%CI: -0.4, 3.7) higher sICAM-1 and sVCAM-1 respectively. No significant associations were observed for black carbon. In interaction models with PM2.5, both sICAM-1 and sVCAM-1 levels were lower in rs1062923 homozygous carriers. These interactions remained significant after multiple comparisons adjustment. Conclusions PM2.5 seven day moving averages are associated with higher sICAM-1 and sVCAM-1 levels. SO4-2 seven day moving averages are associated with higher sICAM-1 and a suggestive association was observed with sVCAM-1 in aging men. SNPs in miRNA-processing genes may modify associations between ambient pollution and sICAM-1 and sVCAM-1, which are correlates of atherosclerosis and cardiovascular disease.

2011-01-01

105

SNPs in the neural cell adhesion molecule 1 gene (NCAM1) may be associated with human neural tube defects  

PubMed Central

Neural tube defects (NTDs) are common birth defects, occurring in approximately 1/1,000 births; both genetic and environmental factors are implicated. To date, no major genetic risk factors have been identified. Throughout development, cell adhesion molecules are strongly implicated in cell–cell interactions, and may play a role in the formation and closure of the neural tube. To evaluate the role of neural cell adhesion molecule 1 (NCAM1) in risk of human NTDs, we screened for novel single-nucleotide polymorphisms (SNPs) within the gene. Eleven SNPs across NCAM1 were genotyped using TaqMan. We utilized a family-based approach to evaluate evidence for association and/or linkage disequilibrium. We evaluated American Caucasian simplex lumbosacral myelomeningocele families (n=132 families) using the family based association test (FBAT) and the pedigree disequilibrium test (PDT). Association analysis revealed a significant association between risk for NTDs and intronic SNP rs2298526 using both the FBAT test (P=0.0018) and the PDT (P=0.0025). Using the HBAT version of the FBAT to look for haplotype association, all pairwise comparisons with SNP rs2298526 were also significant. A replication study set, consisting of 72 additional families showed no significant association; however, the overall trend for overtransmission of the less common allele of SNP rs2298526 remained significant in the combined sample set. In addition, we analyzed the expression pattern of the NCAM1 protein in human embryos, and while NCAM1 is not expressed within the neural tube at the time of closure, it is expressed in the surrounding and later in differentiated neurons of the CNS. These results suggest variations in NCAM1 may influence risk for human NTDs.

Deak, Kristen L.; Boyles, Abee L.; Etchevers, Heather C.; Melvin, Elizabeth C.; Siegel, Deborah G.; Graham, Felicia L.; Slifer, Susan H.; Enterline, David S.; George, Timothy M.; Vekemans, Michel; McClay, David; Bassuk, Alexander G.; Kessler, John A.; Linney, Elwood; Gilbert, John R.

2011-01-01

106

SNPs in the neural cell adhesion molecule 1 gene (NCAM1) may be associated with human neural tube defects.  

PubMed

Neural tube defects (NTDs) are common birth defects, occurring in approximately 1/1,000 births; both genetic and environmental factors are implicated. To date, no major genetic risk factors have been identified. Throughout development, cell adhesion molecules are strongly implicated in cell-cell interactions, and may play a role in the formation and closure of the neural tube. To evaluate the role of neural cell adhesion molecule 1 (NCAM1) in risk of human NTDs, we screened for novel single-nucleotide polymorphisms (SNPs) within the gene. Eleven SNPs across NCAM1 were genotyped using TaqMan. We utilized a family-based approach to evaluate evidence for association and/or linkage disequilibrium. We evaluated American Caucasian simplex lumbosacral myelomeningocele families (n=132 families) using the family based association test (FBAT) and the pedigree disequilibrium test (PDT). Association analysis revealed a significant association between risk for NTDs and intronic SNP rs2298526 using both the FBAT test (P=0.0018) and the PDT (P=0.0025). Using the HBAT version of the FBAT to look for haplotype association, all pairwise comparisons with SNP rs2298526 were also significant. A replication study set, consisting of 72 additional families showed no significant association; however, the overall trend for overtransmission of the less common allele of SNP rs2298526 remained significant in the combined sample set. In addition, we analyzed the expression pattern of the NCAM1 protein in human embryos, and while NCAM1 is not expressed within the neural tube at the time of closure, it is expressed in the surrounding and later in differentiated neurons of the CNS. These results suggest variations in NCAM1 may influence risk for human NTDs. PMID:15883837

Deak, Kristen L; Boyles, Abee L; Etchevers, Heather C; Melvin, Elizabeth C; Siegel, Deborah G; Graham, Felicia L; Slifer, Susan H; Enterline, David S; George, Timothy M; Vekemans, Michel; McClay, David; Bassuk, Alexander G; Kessler, John A; Linney, Elwood; Gilbert, John R; Speer, Marcy C

2005-07-01

107

Vascular cell adhesion molecule 1 expression by biliary epithelium promotes persistence of inflammation by inhibiting effector T-cell apoptosis.  

PubMed

Chronic hepatitis occurs when effector lymphocytes are recruited to the liver from blood and retained in tissue to interact with target cells, such as hepatocytes or bile ducts (BDs). Vascular cell adhesion molecule 1 (VCAM-1; CD106), a member of the immunoglobulin superfamily, supports leukocyte adhesion by binding ?4?1 integrins and is critical for the recruitment of monocytes and lymphocytes during inflammation. We detected VCAM-1 on cholangiocytes in chronic liver disease (CLD) and hypothesized that biliary expression of VCAM-1 contributes to the persistence of liver inflammation. Hence, in this study, we examined whether cholangiocyte expression of VCAM-1 promotes the survival of intrahepatic ?4?1 expressing effector T cells. We examined interactions between primary human cholangiocytes and isolated intrahepatic T cells ex vivo and in vivo using the Ova-bil antigen-driven murine model of biliary inflammation. VCAM-1 was detected on BDs in CLDs (primary biliary cirrhosis, primary sclerosing cholangitis, alcoholic liver disease, and chronic hepatitis C), and human cholangiocytes expressed VCAM-1 in response to tumor necrosis factor alpha alone or in combination with CD40L or interleukin-17. Liver-derived T cells adhered to cholangiocytes in vitro by ?4?1, which resulted in signaling through nuclear factor kappa B p65, protein kinase B1, and p38 mitogen-activated protein kinase phosphorylation. This led to increased mitochondrial B-cell lymphoma 2 accumulation and decreased activation of caspase 3, causing increased cell survival. We confirmed our findings in a murine model of hepatobiliary inflammation where inhibition of VCAM-1 decreased liver inflammation by reducing lymphocyte recruitment and increasing CD8 and T helper 17 CD4 T-cell survival. Conclusions: VCAM-1 expression by cholangiocytes contributes to persistent inflammation by conferring a survival signal to ?4?1 expressing proinflammatory T lymphocytes in CLD. (Hepatology 2014;59:1932-1943). PMID:24338559

Afford, Simon C; Humphreys, Elizabeth H; Reid, Danielle T; Russell, Clare L; Banz, Vanessa M; Oo, Ye; Vo, Tina; Jenne, Craig; Adams, David H; Eksteen, Bertus

2014-05-01

108

Vascular cell-adhesion molecule-1 plays a central role in the proangiogenic effects of oxidative stress  

PubMed Central

Oxidative stress exacerbates neovascularization (NV) in many disease processes. In this study we investigated the mechanism of that effect. Mice deficient in superoxide dismutase 1 (Sod1?/? mice) have increased oxidative stress and show severe ocular NV that is reduced to baseline by antioxidants. Compared with wild-type mice with ischemic retinopathy, Sod1?/? mice with ischemic retinopathy had increased expression of several NF-?B–responsive genes, but expression of vascular cell-adhesion molecule-1 (Vcam1) was particularly high. Intraocular injection of anti–VCAM-1 antibody eliminated the excessive ischemia-induced retinal NV. Elements that contributed to oxidative stress-induced worsening of retinal NV that were abrogated by blockade of VCAM-1 included increases in leukostasis, influx of bone marrow-derived cells, and capillary closure. Compared with ischemia alone, ischemia plus oxidative stress resulted in increased expression of several HIF-1–responsive genes caused in part by VCAM-1–induced worsening of nonperfusion and, hence, ischemia, because anti–VCAM-1 significantly reduced the increased expression of all but one of the genes. These data explain why oxidative stress worsens ischemia-induced retinal NV and may be relevant to other neovascular diseases in which oxidative stress has been implicated. The data also suggest that antagonism of VCAM-1 provides a potential therapy to combat worsening of neovascular diseases by oxidative stress.

Dong, Aling; Shen, Jikui; Zeng, MingBing; Campochiaro, Peter A.

2011-01-01

109

Identification of Intercellular Cell Adhesion Molecule 1 (ICAM-1) as a Hypoglycosylation Marker in Congenital Disorders of Glycosylation Cells*  

PubMed Central

Many human inherited disorders cause protein N-glycosylation defects, but there are few cellular markers to test gene complementation for such defects. Plasma membrane glycoproteins are potential biomarkers because they may be reduced or even absent in plasma membranes of glycosylation-deficient cells. We combined stable isotope labeling by amino acids in cell culture (SILAC) with linear ion trap mass spectrometry (LTQ OrbitrapTM) to identify and quantify membrane proteins from wild-type CHO and glycosylation-deficient CHO (Lec9) cells. We identified 165 underrepresented proteins from 1447 unique quantified proteins, including 18 N-glycosylated plasma membrane proteins. Using various methods, we found that intercellular cell adhesion molecule 1 (ICAM-1) was reduced in Lec9 cells and in fibroblasts from 31 congenital disorder of glycosylation (CDG) patients compared with normal controls. Mannose supplementation of phosphomannose isomerase-deficient CDG-Ib (MPI-CDG) cells and complementation with PMM2 in PMM2-deficient CDG-Ia (PMM2-CDG) cells partially corrected hypoglycosylation based on increased ICAM-1 presence on the plasma membrane. These data indicate that ICAM-1 could be a useful hypoglycosylation biomarker to assess gene complementation of CDG-I patient cells and to monitor improved glycosylation in response to therapeutic drugs.

He, Ping; Ng, Bobby G.; Losfeld, Marie-Estelle; Zhu, Wenhong; Freeze, Hudson H.

2012-01-01

110

Endothelial leukocyte adhesion molecule-1 mediates antigen-induced acute airway inflammation and late-phase airway obstruction in monkeys.  

PubMed Central

This study examines the role of endothelial leukocyte adhesion molecule-1 (ELAM-1) in the development of the acute airway inflammation (cell influx) and late-phase airway obstruction in a primate model of extrinsic asthma. In animals sensitive to antigen, a single inhalation exposure induced the rapid expression of ELAM-1 (6 h) exclusively on vascular endothelium that correlated with the influx of neutrophils into the lungs and the onset of late-phase airway obstruction. In contrast, basal levels of ICAM-1 was constitutively expressed on vascular endothelium and airway epithelium before antigen challenge. After the single antigen exposure, changes in ICAM-1 expression did not correlate with neutrophil influx or the change in airway caliber. This was confirmed by showing that pretreatment with a monoclonal antibody to ICAM-1 did not inhibit the acute influx of neutrophils associated with late-phase airway obstruction, whereas a monoclonal antibody to ELAM-1 blocked both the influx of neutrophils and the late-phase airway obstruction. This study demonstrates a functional role for ELAM-1 in the development of acute airway inflammation in vivo. We conclude that, in primates, the late-phase response is the result of an ELAM-1 dependent influx of neutrophils. Therefore, the regulation of ELAM-1 expression may provide a novel approach to controlling the acute inflammatory response, and thereby, affecting airway function associated with inflammatory disorders, including asthma. Images

Gundel, R H; Wegner, C D; Torcellini, C A; Clarke, C C; Haynes, N; Rothlein, R; Smith, C W; Letts, L G

1991-01-01

111

Endothelial leukocyte adhesion molecule-1 mediates antigen-induced acute airway inflammation and late-phase airway obstruction in monkeys.  

PubMed

This study examines the role of endothelial leukocyte adhesion molecule-1 (ELAM-1) in the development of the acute airway inflammation (cell influx) and late-phase airway obstruction in a primate model of extrinsic asthma. In animals sensitive to antigen, a single inhalation exposure induced the rapid expression of ELAM-1 (6 h) exclusively on vascular endothelium that correlated with the influx of neutrophils into the lungs and the onset of late-phase airway obstruction. In contrast, basal levels of ICAM-1 was constitutively expressed on vascular endothelium and airway epithelium before antigen challenge. After the single antigen exposure, changes in ICAM-1 expression did not correlate with neutrophil influx or the change in airway caliber. This was confirmed by showing that pretreatment with a monoclonal antibody to ICAM-1 did not inhibit the acute influx of neutrophils associated with late-phase airway obstruction, whereas a monoclonal antibody to ELAM-1 blocked both the influx of neutrophils and the late-phase airway obstruction. This study demonstrates a functional role for ELAM-1 in the development of acute airway inflammation in vivo. We conclude that, in primates, the late-phase response is the result of an ELAM-1 dependent influx of neutrophils. Therefore, the regulation of ELAM-1 expression may provide a novel approach to controlling the acute inflammatory response, and thereby, affecting airway function associated with inflammatory disorders, including asthma. PMID:1717514

Gundel, R H; Wegner, C D; Torcellini, C A; Clarke, C C; Haynes, N; Rothlein, R; Smith, C W; Letts, L G

1991-10-01

112

Naringin suppress chondrosarcoma migration through inhibition vascular adhesion molecule-1 expression by modulating miR-126.  

PubMed

Chondrosarcoma, a primary malignant bone cancer, has a potent capacity to invade locally and cause distant metastasis, especially to the lungs. Patients diagnosed with it have poor prognosis. Naringin, polymethoxylated flavonoid commonly found in citrus fruits, has anti-oxidant, anti-inflammatory and anti-tumor activity; whether naringin regulates migration of chondrosarcoma is largely unknown. Here we report that naringin does not expedite apoptosis in human chondrosarcoma. By contrast, at noncytotoxic concentrations, naringin suppressed migration and invasion of chondrosarcoma cells. Vascular cell adhesion molecule-1 (VCAM-1) of the immunoglobulin superfamily is linked with metastasis; we found incubation of chondrosarcoma cells with naringin reducing mRNA transcription for, and cell surface expression of, VCAM-1. We also observed that naringin enhancing miR-126 expression, and miR-126 inhibitor reversed the naringin-inhibited cell motility and VCAM-1 expression. Therefore, naringin inhibits migration and invasion of human chondrosarcoma via down-regulation of VCAM-1 by increasing miR-126. Thus, naringin may be a novel anti-migration agent for the treatment of migration in chondrosarcoma. PMID:24975661

Tan, Tzu-Wei; Chou, Ying-Erh; Yang, Wei-Hung; Hsu, Chin-Jung; Fong, Yi-Chin; Tang, Chih-Hsin

2014-09-01

113

Coxsackievirus A21 binds to decay-accelerating factor but requires intercellular adhesion molecule 1 for cell entry.  

PubMed Central

It is becoming increasingly apparent that many viruses employ multiple receptor molecules in their cell entry mechanisms. The human enterovirus coxsackievirus A21 (CAV21) has been reported to bind to the N-terminal domain of intercellular adhesion molecule 1 (ICAM-1) and undergo limited replication in ICAM-1-expressing murine L cells. In this study, we show that in addition to binding to ICAM-1, CAV21 binds to the first short consensus repeat (SCR) of decay-accelerating factor (DAF). Dual antibody blockade using both anti-ICAM-1 (domain 1) and anti-DAF (SCR1) monoclonal antibodies (MAbs) is required to completely abolish binding and replication of high-titered CAV21. However, the binding of CAV21 to DAF, unlike that to ICAM-1, does not initiate a productive cell infection. The capacity of an anti-DAF (SCR3) MAb to block CAV21 infection but not binding, coupled with immunoprecipitation data from chemical cross-linking studies, indicates that DAF and ICAM-1 are closely associated on the cell surface. It is therefore suggested that DAF may function as a low-affinity attachment receptor either enhancing viral presentation or providing a viral sequestration site for subsequent high-affinity binding to ICAM-1.

Shafren, D R; Dorahy, D J; Ingham, R A; Burns, G F; Barry, R D

1997-01-01

114

Intracellular Adhesion Molecule-1 K469E Gene Polymorphism and Risk of Diabetic Microvascular Complications: A Meta-Analysis  

PubMed Central

Background A number of studies evaluated the association of intracellular adhesion molecule-1 (ICAM-1) K469E (rs5498, A/G) gene polymorphism with diabetic microvascular complications (DMI) including diabetic nephropathy (DN) and diabetic retinopathy (DR) in different populations. However, the results of individual studies remain conflicting. Methods A comprehensive search was conducted to identify all eligible studies of the above-mentioned associations. The pooled odds ratios (ORs) and 95% confidence intervals (CIs) were assessed using the fixed or random effect model. Results Seven studies involving 3411 subjects were included. Overall, the meta-analysis showed a significant association of the A allele with increased risk of DMI susceptibility in a recessive model (OR?=?1.37, 95% CI 1.04–1.80, P?=?0.02). In the subgroup analysis stratified by ethnicity, significant association was found in Asians but not in Caucasians (OR?=?1.78, 95% CI 1.13–2.81, P?=?0.01; OR?=?1.10, 95% CI 0.79–1.54, P?=?0.58, respectively). Moreover, it showed a significant association between the A allele and risk of DN in a recessive model (OR?=?1.25, 95% CI 1.02–1.55, P?=?0.04). Conclusions This meta-analysis suggested that the K469E polymorphism in ICAM-1 gene might affect individual susceptibility to DMI and showed a discrepancy in different ethnicities. Further investigations are needed to validate the association.

Su, Xianghui; Chen, Xi; Liu, Lei; Chang, Xiangyun; Yu, Xuefeng; Sun, Kan

2013-01-01

115

5,7-Dihydroxy-3,4,6-trimethoxyflavone inhibits intercellular adhesion molecule 1 and vascular cell adhesion molecule 1 via the Akt and nuclear factor-?B-dependent pathway, leading to suppression of adhesion of monocytes and eosinophils to bronchial epithelial cells  

PubMed Central

5,7-Dihydroxy-3?,4?,6?-trimethoxyflavone (eupatilin), the active pharmacological ingredient from Artemisia asiatica Nakai (Asteraceae), is reported to have a variety of anti-inflammatory properties in intestinal epithelial cells. However, little information is known about the molecular mechanism of eupatilin-induced attenuation of bronchial epithelial inflammation. This study investigates the role of eupatilin in the adhesion of inflammatory cells such as monocytes and eosinophils to bronchial epithelial cells. Stimulation of a human bronchial epithelial cell line (BEAS-2B) with tumour necrosis factor-? (TNF-?) increased the expression of surface adhesion molecules, including intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), in which eupatilin significantly inhibited the expression of those adhesion molecules in a dose-dependent manner. Eupatilin suppressed the TNF-?-induced activation of I?B? and nuclear factor-?B (NF-?B) signals in BEAS-2B cells. The I?B kinase (IKK) activation was also significantly reduced in eupatilin-pre-treated BEAS-2B and primary normal human bronchial epithelial (NHBE) cells. However, eupatilin did not influence AP-1 activity in TNF-?-stimulated cells. Suppression of NF-?B signalling induced by eupatilin resulted in the inhibition of the expression of adhesion molecules and the adhesion of monocytes and eosinophils to BEAS-2B cells. Furthermore, eupatilin suppressed the phosphorylation of Akt in TNF-?-stimulated BEAS-2B and NHBE cells, leading to down-regulation of NF-?B activation and adhesion molecule expression and finally to suppression of the inflammatory cell adhesion to epithelial cells. These results suggest that eupatilin can inhibit the adhesion of inflammatory cells to bronchial epithelial cells via a signalling pathway, including activation of Akt and NF-?B, as well as expression of adhesion molecules.

Jung, Jireh; Ko, Su H; Yoo, Do Y; Lee, Jin Y; Kim, Yeong-Jeon; Choi, Seul M; Kang, Kyung K; Yoon, Ho J; Kim, Hyeyoung; Youn, Jeehee; Kim, Jung M

2012-01-01

116

Inhibitor of differentiation is overexpressed with progression of benign to malignant lesions and related with carcinoembryonic antigen–related cell adhesion molecule 1 distribution in mammary glands  

Microsoft Academic Search

The purpose of the study was to investigate the expression and association of inhibitor of differentiation (Id-1) and carcinoembryonic antigen–related cell adhesion molecule 1 (CEACAM1) in benign, premalignant, and malignant lesions of human mammary glands. The study included 97 cases of benign, premalignant, and malignant lesions of human mammary glands including normal terminal duct lobular units, usual ductal hyperplasia, atypical

Qian Liu; Yong-Mei Yang; Qing-hui Zhang; Ting-guo Zhang; Qinghua Zhou; Cheng-jun Zhou

2011-01-01

117

Wiskott-Aldrich syndrome protein controls antigen-presenting cell-driven CD4+ T-cell motility by regulating adhesion to intercellular adhesion molecule-1  

PubMed Central

T-cell scanning for antigen-presenting cells (APC) is a finely tuned process. Whereas non-cognate APC trigger T-cell motility via chemokines and intercellular adhesion molecule-1 (ICAM-1), cognate APC deliver a stop signal resulting from antigen recognition. We tested in vitro the contribution of the actin cytoskeleton regulator Wiskott–Aldrich syndrome protein (WASP) to the scanning activity of primary human CD4+ T cells. WASP knock-down resulted in increased T-cell motility upon encounter with non-cognate dendritic cells or B cells and reduced capacity to stop following antigen recognition. The high motility of WASP-deficient T cells was accompanied by a diminished ability to round up and to stabilize pauses. WASP-deficient T cells migrated in a normal proportion towards CXCL12, CCL19 and CCL21, but displayed an increased adhesion and elongation on ICAM-1. The elongated morphology of WASP-deficient T cells was related to a reduced confinement of high-affinity lymphocyte function-associated antigen 1 to the mid-cell zone. Our data therefore indicate that WASP controls CD4+ T-cell motility upon APC encounter by regulating lymphocyte function-associated antigen 1 spatial distribution.

Lafouresse, Fanny; Cotta-de-Almeida, Vinicius; Malet-Engra, Gema; Galy, Anne; Valitutti, Salvatore; Dupre, Loic

2012-01-01

118

Effects of a thrombomodulin-derived peptide on monocyte adhesion and intercellular adhesion molecule-1 expression in lipopolysaccharide-induced endothelial cells  

PubMed Central

Purpose It has been documented that GC31, a 31-animo acid peptide from human thrombomodulin, has potent anti-inflammatory properties in endotoxin-induced uveitis and lipopolysaccharide (LPS)-induced RAW264.7 cells, while the role of GC31 in the endothelial cells has not yet been fully understood. Therefore, the aim of this study was to explore the effect of GC31 on intercellular adhesion molecule-1 (ICAM-1) expression in LPS-activated endothelial cells. Methods Human umbilical vein endothelial cells (HUVECs) were incubated with LPS (1 ?g/ml) and peptide GC31 or control peptide VP30 simultaneously. ICAM-1 messenger RNA and protein levels were evaluated with real-time PCR and western blot. The adhesion of U937 cells labeled with CM-H2DCFDA to HUVECs was examined with ?uorescence microscope. Extracellular signal-regulated kinase-1/2 (ERK1/2) and p38 mitogen-activated protein kinase (MAPK) activation, inhibitor of nuclear factor kappa B alpha (I?B?) degradation, and nuclear factor kappa B (NF-?B) nuclear translocation were detected with western blot. Results Upon LPS stimulation, GC31 suppressed the mRNA and protein expression of ICAM-1 in HUVECs and remarkably reduced monocyte-endothelial cell adhesion in a dose-dependent manner. Furthermore, GC31 significantly inhibited the degradation of I?B? and nuclear translocation of NF-?B and moderately blocked the activation of p38 MAPK and ERK1/2 in activated HUVECs. Conclusions Our results suggested that GC31 suppressed LPS-mediated ICAM-1 expression by inhibiting the activation of NF-?B and partially by attenuating the activity of ERK1/2 and p38 MAPK in vascular endothelium, which may contribute to ameliorating vascular inflammatory diseases, such as uveitis.

Xu, Yan; Xu, Xun; Yang, Xiaolu; Gu, Qing; Liu, Kun

2013-01-01

119

Clinical significance of serum epithelial cell adhesion molecule (EPCAM) and vascular cell adhesion molecule-1 (VCAM-1) levels in patients with epithelial ovarian cancer.  

PubMed

Cellular adhesion molecules might be good markers in some types of malignant tumors, useful information in diagnosis and prognosis. The objective of this study was to evaluate the serum levels of epithelial cell adhesion molecule (EPCAM) and vascular cell adhesion molecule-1 (VCAM-1) in epithelial ovarian cancer (EOC) patients. Fifty patients were enrolled into the study. Serum EPCAM and VCAM-1 levels were determined by the solid-phase sandwich ELISA method. Age- and sex-matched 30 healthy controls were included in the analysis. The median age of the patients was 56.5 years, range 22 to 83 years. Majority of the patients had advanced disease (stages III-IV) (90%). The baseline serum EPCAM levels of the EOC patients were significantly higher than in those in the control group (p = 0.03). However, there was no significant difference in the serum VCAM-1 level between EOC patients and controls (p = 0.24). Metastatic patients had higher serum VCAM-1 levels compared with the non-metastatic patients (p = 0.03). Moreover, no other clinical variables including response to chemotherapy were found to be correlated with both serum assays (p > 0.05). No correlation was found between serum EPCAM and VCAM-1 levels in EOC patients (r(s) = 0.105, p = 0.362). Neither serum EPCAM level nor serum VCAM-1 level had significant adverse effect on survival. In conclusion, the higher baseline serum levels of VCAM-1 were associated with metastatic disease, and serum EPCAM level was found to be a diagnostic marker in EOC patients. However, both serum assays had no prognostic roles on outcome. PMID:24307621

Tas, Faruk; Karabulut, Senem; Serilmez, Murat; Ciftci, Rumeysa; Duranyildiz, Derya

2014-04-01

120

Keratinocyte intercellular adhesion molecule-1 (ICAM-1) expression precedes dermal T lymphocytic infiltration in allergic contact dermatitis (Rhus dermatitis).  

PubMed

The ability of small molecules such as urushiol, present as a wax on the poison ivy leaf surface, to cause allergic contact dermatitis (rhus dermatitis) has fascinated immunologists for decades. Current dogma suggests that these epicutaneously applied catechol-containing molecules serve as haptens to conjugate with larger proteins via reactive o-quinone intermediates. These complexes are then recognized as foreign antigens by the immune system and elicit a hypersensitivity reaction. Phorbol ester can directly induce cultured keratinocyte (KC) intercellular adhesion molecule-1 (ICAM-1) expression via a protein kinase C (PK-C)-dependent mechanism. As urushiol is also a known PK-C agonist, we asked if topical application of a poison ivy/oak mixture could directly induce epidermal KC ICAM-1 expression. During the pre-erythematous phase of this reaction (4 to 20 hours), epidermal KCs expressed ICAM-1; this "initiation phase" preceded the appearance of activated memory T lymphocytes in the papillary dermis, and thus appeared to be nonlymphokine mediated. A near-contiguous cellular-adhesion molecular network was identified by ICAM-1 staining of basal KCs, dermal dendrocytes, and endothelial cells. During the second 24-hour period with the onset of erythema and edema, there was an "amplification phase" of more intense KC ICAM-1 expression coupled with relatively weak KC HLA-DR expression that coincided with dermal and epidermal T-cell infiltration. This suggests the presence of lymphokines, such as gamma interferon, during the amplification phase because of KC HLA-DR expression. On cultured KCs, urushiol directly induced ICAM-1 expression but not HLA-DR. Thus, in addition to functioning as an antigenic hapten, urushiol directly induces KC ICAM-1 expression. The KC ICAM-1 expression may then alter the dynamic trafficking of memory T cells in the epidermis, so as to initiate cutaneous inflammation in a nonantigen specific manner. This initiation phase is followed by T-cell infiltration and consequent lymphokine production that significantly amplifies the original stimulus. Thus much can still be learned about the molecular pathophysiology of this common type of cutaneous inflammation. PMID:2574536

Griffiths, C E; Nickoloff, B J

1989-12-01

121

Keratinocyte intercellular adhesion molecule-1 (ICAM-1) expression precedes dermal T lymphocytic infiltration in allergic contact dermatitis (Rhus dermatitis).  

PubMed Central

The ability of small molecules such as urushiol, present as a wax on the poison ivy leaf surface, to cause allergic contact dermatitis (rhus dermatitis) has fascinated immunologists for decades. Current dogma suggests that these epicutaneously applied catechol-containing molecules serve as haptens to conjugate with larger proteins via reactive o-quinone intermediates. These complexes are then recognized as foreign antigens by the immune system and elicit a hypersensitivity reaction. Phorbol ester can directly induce cultured keratinocyte (KC) intercellular adhesion molecule-1 (ICAM-1) expression via a protein kinase C (PK-C)-dependent mechanism. As urushiol is also a known PK-C agonist, we asked if topical application of a poison ivy/oak mixture could directly induce epidermal KC ICAM-1 expression. During the pre-erythematous phase of this reaction (4 to 20 hours), epidermal KCs expressed ICAM-1; this "initiation phase" preceded the appearance of activated memory T lymphocytes in the papillary dermis, and thus appeared to be nonlymphokine mediated. A near-contiguous cellular-adhesion molecular network was identified by ICAM-1 staining of basal KCs, dermal dendrocytes, and endothelial cells. During the second 24-hour period with the onset of erythema and edema, there was an "amplification phase" of more intense KC ICAM-1 expression coupled with relatively weak KC HLA-DR expression that coincided with dermal and epidermal T-cell infiltration. This suggests the presence of lymphokines, such as gamma interferon, during the amplification phase because of KC HLA-DR expression. On cultured KCs, urushiol directly induced ICAM-1 expression but not HLA-DR. Thus, in addition to functioning as an antigenic hapten, urushiol directly induces KC ICAM-1 expression. The KC ICAM-1 expression may then alter the dynamic trafficking of memory T cells in the epidermis, so as to initiate cutaneous inflammation in a nonantigen specific manner. This initiation phase is followed by T-cell infiltration and consequent lymphokine production that significantly amplifies the original stimulus. Thus much can still be learned about the molecular pathophysiology of this common type of cutaneous inflammation. Images Figure 2 Figure 3 Figure 4 Figure 5 Figure 6 Figure 7 Figure 8 Figure 9

Griffiths, C. E.; Nickoloff, B. J.

1989-01-01

122

Engineering of Single Ig Superfamily Domain of Intercellular Adhesion Molecule 1 (ICAM-1) for Native Fold and Function*  

PubMed Central

The immunoglobulin (Ig) superfamily is one of the largest families in the vertebrate genome, found most frequently in cell surface molecules. Intercellular adhesion molecule-1 (ICAM-1) contains five extracellular Ig superfamily domains (D1-D5) of which the first domain, D1, is the binding site for the integrin lymphocyte function-associated antigen-1 (LFA-1) and human rhinovirus. Despite the modular nature of many Ig superfamily domains with respect to domain folding and ligand recognition, D1 does not fold on its own due to the loss of its interaction with the second domain. The goal of this study was to engineer ICAM-1 D1 by introducing mutations that would stabilize the Ig superfamily domain fold while retaining its ability to bind to LFA-1 and rhinovirus. First, with a directed evolution approach, we isolated mutations in D1 that showed binding to conformation-specific antibodies and the ligand binding domain of LFA-1 called the inserted, or I, domain. Then, with a rational design approach we introduced mutations that contributed to the stability of ICAM-1 D1 in solution. The mutations that restored native folding of D1 in isolation were those that would convert hydrogen bond networks in buried regions into hydrophobic contacts. Notably, for most mutations, identical or similar types of substitutions were found in ICAM-1 molecules of different species and other ICAM family members. The systematic approach demonstrated in this study to engineer a single Ig superfamily fold in ICAM-1 can be broadly applicable to the engineering of modular Ig superfamily domains in other cell surface molecules.

Owens, Roisin M.; Gu, Xiaoling; Shin, Miran; Springer, Timothy A.; Jin, Moonsoo M.

2010-01-01

123

Plasma zinc levels inversely correlate with vascular cell adhesion molecule-1 concentration in children with sickle cell disease.  

PubMed Central

Zinc deficiency has been implicated in impaired cell-mediated immunity of children with sickle cell disease (SCD). However, its influence on the expression of vascular cell-adhesion molecule-1 (VCAM-1) on endothelial cells, a protein involved in vasoocclusion, has not been previously investigated. We therefore measured (soluble) sVCAM-1 and zinc in 76 SCD children and 96 non-SCD children, mean age 7.73 years and 11.24 years, respectively. Although mean zinc levels of both groups were within the normal range (approximately 14.5 micromol/l), 14.5 % of SCD and 11% of non-SCD children (without inflammation) had levels below normal (10.7 micromol/L). Mean sVCAM-1 concentrations of SCD children (837 microg/l) were significantly higher than those of controls (627 microg/l) (p < 0.001). Differences persisted after taking into account age, hemoglobin phenotype, and inflammation (alpha-l acid glycoprotein >l g/l and C-reactive protein >10 mg/I). sVCAM-1 negatively correlated with serum (r = -0.444) and red blood cells zinc (r = -0.242, p < 0.05) but not with acute-phase proteins. Mean sVCAM-1 tended to be higher in SCD children with than in those without a history of a health problem (infection, pain crisis or were transfused; not significant). Data suggest that zinc may modulate the clinical status of SCD children through VCAM-1 expression, and zinc supplementation may be beneficial in these patients.

Kuvibidila, Solo R.; Sandoval, Manuel; Lao, Juan; Velez, Maria; Yu, Lolie; Ode, David; Gardner, Renee; Lane, Gerald; Warrier, Raj P.

2006-01-01

124

Substance P plays an important role in cell adhesion molecule 1-mediated nerve-pancreatic islet ? cell interaction.  

PubMed

Autonomic neurons innervate pancreatic islets of Langerhans and maintain blood glucose homeostasis by regulating hormone levels. We previously showed that cell adhesion molecule 1 (CADM1) mediated the attachment and interaction between nerves and aggregated pancreatic islet ? cells. In this study, we cocultured ?TC6 cells, a murine ? cell line, with mouse superior cervical ganglion (SCG) neurons. The oscillation of intracellular Ca(2+) concentration ([Ca(2+)]i) was observed in 27% and 14% of ?TC6 and CADM1-knockdown ?TC6 cells (?TC6(siRNA-CADM1) cells) in aggregates, respectively, within 1min after specific SCG nerve stimulation with scorpion venom. In ?TC6(siRNA-CADM1) cells, the responding rate during 3min after SCG nerve stimulation significantly increased compared with that within 1min, whereas the increase in the responding rate was not significantly different in ?TC6 cells. This indicated that the response of ?TC6 cells according to nerve stimulation occurred more rapidly and effectively than that of ?TC6(siRNA-CADM1) cells, suggesting CADM1 involvement in promoting the interaction between nerves and ? cells and among ? cells. In addition, because we found that neurokinin (NK)-1 receptors, which are neuropeptide substance P receptors, were expressed to a similar extent by both cells, we investigated the effect of substance P on nerve-? cell interaction. Pretreatment with CP99,994 (0.1?g/ml), an NK-1 receptor antagonist, reduced the responding rate of both cells, suggesting that substance P released from stimulated neurites was a mediator to activate ?TC6 cells. In addition, ? cells that were attached to neurites in a CADM1-mediated manner appeared to respond effectively to neurite activation via substance P/NK-1 receptors. PMID:23899526

Nakamura, Mami; Inoh, Yoshikazu; Nakanishi, Mamoru; Furuno, Tadahide

2013-08-30

125

Prediction value of intercellular adhesion molecule-1 gene polymorphisms for epithelial ovarian cancer risk, clinical features, and prognosis.  

PubMed

Intercellular adhesion molecule-1 (ICAM-1, encoded by ICAM-1) is implicated in tumorigenesis and tumor progression. ICAM-1 modulates the susceptibility to several types of cancer and the disease prognosis; however, its role in epithelial ovarian cancer (EOC) is unclear. Here, we evaluate single nucleotide polymorphisms (SNPs) in ICAM-1 as predictors of EOC risk and prognosis. Six ICAM-1 polymorphisms were genotyped in 408 patients with EOC and 520 controls using the MassARRAY system. The ICAM-1 mRNA levels in 89 EOC tissues and 35 normal ovarian tissues were examined using quantitative PCR. The ICAM-1 rs5498 G allele was associated with increased tumor grade (OR=2.650) and EOC risk (OR=1.405). This risk was more evident in females who had first-degree relatives (FDRs) with a tumor (OR=3.475) or who experienced early menarche (OR=2.774). The ICAM-1 expression in the cancerous tissue was elevated compared with that of normal ovarian tissues (p<0.0001), and it was associated with an rs5498 genotype (p=0.0002). ICAM-1 SNPs did not significantly predict the overall EOC survival (p>0.05). However, the rs5498 G allele correlated with EOC survival time in patients whose FDRs suffered from a tumor (p=0.001). ICAM-1 rs5498 likely confers a high risk for EOC in G allele carriers accompanied by up-regulation of ICAM-1 expression during carcinogenesis. The combination of ICAM-1 rs5498 and tumor history predicts the EOC prognosis. PMID:23933413

Cai, Guoqing; Ma, Xiangdong; Zou, Wei; Huang, Yanhong; Zhang, Junru; Wang, Detang; Chen, Biliang

2014-08-01

126

Prognostic prediction and diagnostic role of intercellular adhesion molecule-1 (ICAM1) expression in clear cell renal cell carcinoma.  

PubMed

The intercellular adhesion molecule-1 (ICAM1) has been reported to function in multiple malignancies, but its effect on clear cell renal cell carcinoma (ccRCC) hasn't been discussed yet. This study aimed to identify the potential role of ICAM1 in prognostic prediction and early diagnosis of ccRCC. ICAM1 expression was inspected by immunohistochemistry and correlated with clinicopathologic variables. Association between protein expression and cancer-specific survival (CSS) of ccRCC patients was evaluated and the value of area under the receiver operating characteristics (ROC) curve (AUC) was calculated to measure the protein's diagnostic accuracy. ICAM1 was positively immunostained in 83.2 % of 173 ccRCC tissues, but negatively immunostained in all the para-cancerous normal epitheliums of renal tubules. High ICAM1 expression was significantly related to male sex (P = 0.00241), T3/T4 stage (P = 0.02249), non-N0M0 stage (P = 0.03797) and positive renal pelvis invasion (P = 0.04227). Kaplan-Meier survival analysis illustrated that high ICAM1 expression was significantly correlated to a decreased CSS (P = 0.00006). Multivariate Cox analysis indicated that ICAM1 was an independent predictor for CSS of patients (P = 0.00451). Furthermore, the AUC value of ICAM1 in diagnosing ccRCC was 0.916 (P < 0.00001). In conclusion, high ICAM1 expression on tumor cells indicates a poor outcome of patients and ICAM1 is likely to be an independent predictor for the prognosis of ccRCC. Moreover, ICAM1 has a high AUC value and may be a potential and useful diagnostic marker. PMID:24535541

Shi, Xuebing; Jiang, Jifa; Ye, Xiaobing; Liu, Yanyan; Wu, Qiong; Wang, Lu

2014-08-01

127

Pentoxifylline in vivo and in vitro down-regulates the expression of the intercellular adhesion molecule-1 in monocytes.  

PubMed Central

Since pentoxifylline (PTX) was recently recognized as a substance with antiinflammatory capacities, we studied the in vivo and in vitro effect of PTX on the expression of the intercellular adhesion molecule-1 (ICAM-1) on human monocytes. For this purpose four healthy volunteers were treated with PTX (5 x 400 mg/day) for 2 days. Monocytes were isolated before and after PTX treatment and ICAM-1 expression was investigated. As shown by fluorescence-activated cell sorter (FACS) analysis, cultured monocytes isolated after oral application of PTX expressed significantly decreased amounts of ICAM-1 when compared with monocytes collected prior to oral PTX application. Northern blot analysis revealed reduced amounts of ICAM-1 mRNA in monocytes derived from volunteers after oral PTX treatment in comparison with monocytes isolated before oral PTX administration. Similarly, in monocytes treated with PTX (200 micrograms/ml) in vitro ICAM-1 was found decreased both at the protein and mRNA level in comparison with untreated cells. The inhibitory effect of PTX on ICAM-1 expression in monocytes could be reversed by the addition of exogenous tumour necrosis factor-alpha (TNF-alpha; 200 U/ml) suggesting that ICAM-1 down-regulation is mediated secondary to TNF-alpha suppression by PTX. The specific role of TNF-alpha in mediating ICAM-1 expression in cultured monocytes could be confirmed by the finding that a neutralizing anti-TNF-alpha antibody partially down-regulated ICAM-1 expression. The observed suppressive in vivo and in vitro effects of PTX on ICAM-1 expression in monocytes may contribute to the recently described antiinflammatory effects of PTX, e.g. in sepsis or allergic contact dermatitis. Images Figure 2 Figure 5

Neuner, P; Klosner, G; Pourmojib, M; Knobler, R; Schwarz, T

1997-01-01

128

The different expression of carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) and possible roles in gastric carcinomas.  

PubMed

The purpose of this study was to investigate the expression of carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) and its effects on promoting angiogenesis in gastric adenocarcinomas. Paraffin wax sections of 222 patients with gastric adenocarcinomas having undergone surgery between 2001 and 2006 were classified into three histotypes: intestinal, diffuse, and mixed carcinomas following the Laurén classification. Immunohistochemistry (IHC) was used to study the distribution of CEACAM1, and double-labeling immunohistochemistry was used to observe the relationship between CEACAM1 expression and neovascularization in carcinoma areas. No CEACAM1 expression was found in normal non-metaplastic mucosa adjacent to the tumors; but in metaplastic mucosa, CEACAM1 was expressed on the apical surface. However, all of the collected gastric carcinomas expressed CEACAM1 with cytoplasmic or membranous staining. CEACAM1 was expressed mainly with a membranous pattern in the intestinal carcinomas, and with a cytoplasmic pattern in the diffuse carcinomas. There was a significant difference between the expression patterns and the histotypes (P<0.0001). CEACAM1 expression was classified as high (> or =66% positive cells) and low (<66% positive cells), and high CEACAM1 expression was associated with lymph nodes metastasis (P<0.05). High microvessel density (MVD) was observed more frequently in the tumors with membranous expression, and low MVD in the tumors with cytoplasmic staining (P<0.0001). The transformation of CEACAM1 distribution from membrane to cytoplasm is an important incident for the reverse effects on the tumorous angiogenesis, and high expression of CEACAM1 facilitates the metastasis of carcinoma cells to lymph nodes. Moreover, the different distribution of CEACAM1 in the intestinal and diffuse carcinomas indicates a different tumorigenic pathway. PMID:19243897

Zhou, Cheng-Jun; Liu, Bin; Zhu, Kong-Xi; Zhang, Qing-Hui; Zhang, Ting-Guo; Xu, Wei-Hua; Wang, Hong-Bo; Yu, Wei-Hua; Qu, Yun-Dong; Wang, Hong-Juan; Wu, Hong-Li; Sun, Shan-Zhen; Guo, Jian-Qiang

2009-01-01

129

Immunologic changes in TNF-alpha, sE-selectin, sP-selectin, sICAM-1, and IL-8 in pediatric patients treated for psoriasis with the Goeckerman regimen  

SciTech Connect

Psoriasis is a chronic inflammatory skin disease which is often manifested during childhood. The present study investigated changes in the serum levels of proinflammatory cytokines and soluble forms of adhesion molecules in children with psoriasis. The observed patient group of 26 children was treated with the Goeckerman regimen. This therapy combines dermal application of crude coal tar with ultraviolet radiation. The Psoriasis Area Severity Index decreased significantly after treatment by with the Goeckerman regimen (p < 0.001). Serum levels of the proinflammatory cytokine TNF-alpha and adhesion molecules sICAM-1, sP-selectin and sE-selectin decreased after the Goeckerman regimen. The TNF-alpha and sICAM-1 decreased significantly (p < 0.05). Our findings support the complex role of these immune parameters in the immunopathogenesis of psoriasis in children. The serum level of IL-8 increased after the Goeckerman regimen. This fact indicates that the chemokine pathway of IL-8 activity could be modulated by this treatment, most likely by polycyclic aromatic hydrocarbons.

Borska, L.; Fiala, Z.; Krejsek, J.; Andrys, C.; Vokurkova, D.; Hamakova, K.; Kremlacek, J.; Ettler, K. [Charles University of Prague, Hradec Kralove (Czech Republic). Faculty of Medicine

2007-11-15

130

Insulin sensitivity, plasma adiponectin and sICAM-1 concentrations in patients with subclinical hypothyroidism: response to levothyroxine therapy  

Microsoft Academic Search

Subclinical hypothyroidism is associated with an increased risk of atherosclerosis. The aim of this study was to investigate\\u000a the concentration of plasma soluble intercellular adhesion molecule-1 and adiponectin in relation to insulin sensitivity in\\u000a patients with subclinical hypothyroidism and to estimate if l-thyroxine treatment had an influence on these parameters. 13 women with subclinical hypothyroidism and 14 euthyroid controls\\u000a were

Irina Kowalska; Jacek Borawski; Agnieszka Niko?ajuk; Tadeusz Budlewski; El?bieta Otziomek; Maria Górska; Marek Str?czkowski

131

Angiotensin II Induces Vascular Cell Adhesion Molecule1 Expression In Rat Vasculature A Potential Link Between the Renin-Angiotensin System and Atherosclerosis  

Microsoft Academic Search

Background—Cardiovascular ischemic events may occur more frequently in hypertensive patients with activated renin-angiotensin systems. We tested the hypothesis that angiotensin II (Ang II) may contribute to atherosclerosis by increasing expression of vascular inflammatory genes such as vascular cell adhesion molecule-1 (VCAM-1). Methods and Results—Rats infused with norepinephrine or Ang II for 6 days developed similar hypertensive responses, but only Ang

Pradyumna E. Tummala; Xi-Lin Chen; Cynthia L. Sundell; Jørn Bech Laursen; C. Patricia Hammes; R. Wayne Alexander; David G. Harrison; Russell M. Medford

132

Increase in interleukin-8 and soluble intercellular adhesion molecule-1 in bronchoalveolar lavage fluid from premature infants who develop chronic lung disease  

Microsoft Academic Search

Interleukin-8 (IL-8), soluble intercellular adhesion molecule-1 (sICAM), elastase and neutrophils were assessed in bronchoalveolar lavage fluid from nine infants who developed chronic lung disease (CLD) after respiratory distress syndrome (RDS), seven who had recovered from RDS, and in four control infants. IL-8, sICAM, elastase and neutrophils in bronchoalveolar lavage fluid were increased in the CLD group, the differences being most

S. Kotecha; B. Chan; N. Azam; M. Silverman; R. J. Shaw

1995-01-01

133

Immunoultrastructural expression of intercellular adhesion molecule-1 in endothelial cell vesiculotubular structures and vesiculovacuolar organelles in blood-brain barrier development and injury  

Microsoft Academic Search

Blood vessels from the vasculature of mouse brains during postnatal development and from human brain tumors (hemangiomas) removed at biopsy were examined immunocytochemically by transmission electron microscopy (TEM) or high-voltage transmission electron microscopy (HVEM) to determine the expression of intercellular adhesion molecule-1 (ICAM-1). In the mouse brains, ICAM-1 was shown to be initially expressed on the luminal and abluminal endothelial

A. S. Lossinsky; K. F. Buttle; R. Pluta; M. J. Mossakowski; H. M. Wi?niewski

1999-01-01

134

GroEL1, from Chlamydia pneumoniae, Induces Vascular Adhesion Molecule 1 Expression by p37AUF1 in Endothelial Cells and Hypercholesterolemic Rabbit  

Microsoft Academic Search

The expression of vascular adhesion molecule-1 (VCAM-1) by endothelial cells may play a major role in atherogenesis. The actual mechanisms of chlamydia pneumoniae (C. pneumoniae) relate to atherogenesis are unclear. We investigate the influence of VCAM-1 expression in the GroEL1 from C. pneumoniae-administered human coronary artery endothelial cells (HCAECs) and hypercholesterolemic rabbits. In this study, we constructed the recombinant GroEL1

Chun-Yao Huang; Chun-Ming Shih; Nai-Wen Tsao; Yung-Hsiang Chen; Chi-Yuan Li; Yu-Jia Chang; Nen-Chung Chang; Keng-Liang Ou; Cheng-Yen Lin; Yi-Wen Lin; Chih-Hao Nien; Feng-Yen Lin

2012-01-01

135

Identification of Fer Tyrosine Kinase Localized on Microtubules as a Platelet Endothelial Cell Adhesion Molecule1 Phosphorylating Kinase in Vascular Endothelial Cells  

Microsoft Academic Search

Platelet endothelial adhesion molecule-1 (PECAM-1) is a part of intercellular junctions and triggers intracellular signaling cascades upon homophilic binding. The intracellular domain of PECAM-1 is tyrosine phosphorylated upon homophilic engagement. However, it remains unclear which tyrosine kinase phosphorylates PECAM-1. We sought to isolate tyrosine kinases respon- sible for PECAM-1 phosphorylation and identified Fer as a candidate, based on expression cloning.

Naoko Kogata; Michitaka Masuda; Yuji Kamioka; Akiko Yamagishi; Akira Endo; Masato Okada; Naoki Mochizuki

2003-01-01

136

Four new clerodane diterpenes from the leaves of Casearia guianensis which inhibit the interaction of leukocyte function antigen 1 with intercellular adhesion molecule 1.  

PubMed

Four new clerodane diterpenes, casearinols A and B (1 and 2) and casearinones A and B (3 and 4), were isolated from the leaves of Casearia guianensis. These immunomodulatory compounds have been structurally elucidated primarily on the basis of 2D NMR analysis and spectral data comparison with known compounds. These compounds inhibited the binding of T-cell leukocyte function antigen 1 to intercellular adhesion molecule 1. PMID:9322361

Hunter, M S; Corley, D G; Carron, C P; Rowold, E; Kilpatrick, B F; Durley, R C

1997-09-01

137

Nitric Oxide Regulates Vascular Cell Adhesion Molecule 1 Gene Expression and Redox-Sensitive Transcriptional Events in Human Vascular Endothelial Cells  

Microsoft Academic Search

Decreased nitric oxide (NO) activity, the formation of reactive oxygen species, and increased endothelial expression of the redox-sensitive vascular cell adhesion molecule 1 (VCAM-1) gene in the vessel wall are early and characteristic features of atherosclerosis. To explore whether these phenomena are functionally interrelated, we tested the hypothesis that redox-sensitive VCAM-1 gene expression is regulated by a NO-sensitive mechanism. In

Bobby V. Khan; David G. Harrison; Matthew T. Olbrych; R. Wayne Alexander; Russell M. Medford

1996-01-01

138

The influence of volume therapy and pentoxifylline infusion on circulating adhesion molecules in trauma patients.  

PubMed

Adhesion molecules appear to play a pivotal role in tissue damage secondary to the inflammatory process. Besides neutrophil- and endothelial-bound adhesion molecules, soluble forms have been detected in the circulating blood. They seem to be good markers of endothelial damage, but they may also have other biological functions. Plasma concentrations of soluble adhesion molecules (endothelial leucocyte adhesion molecules (sELAM-1), intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (sVCAM-1), and granule membrane protein 140 (sGMP-140) were serially measured over 5 days by enzyme-linked immunosorbent assays (ELISA) in 45 consecutive trauma patients. These received, by random allocation, only either hydroxyethylstarch solution 10% (mean molecular weight 200,000 daltons) (n = 15) or human albumin 20% (n = 15) for volume therapy. Another 15 patients without defined volume therapy received pentoxifylline continuously (1.2 mg.kg-1.h-1). Measurements were carried out on the day of admission to the intensive care unit (baseline) and during the next 5 days. At baseline, plasma concentrations of all adhesion molecules were similar in all groups. In the hydroxyethyl starch group, sELAM-1 and sICAM-1 concentrations decreased significantly (p < 0.05) reaching normal values during the study period whereas the mean (SD) values increased in the pentoxifylline group (sELAM-1: 71.1 (16.7) to 91.6 (17.8) ng.ml-1) and the albumin group (sICAM-1: 400 (81) to 749 (101) ng.ml-1) (p < 0.05). sVCAM-1 increased outside the normal range only in the human albumin group (to 760 +/- 69 ng.ml-1) (p < 0.05). sGMP-140 plasma concentration increased only in those receiving albumin (432 (85) to 550 (93) ng.ml-1) and this was significantly different to the other groups (p < 0.05). None of the other haemodynamic or laboratory factors could be correlated with plasma concentrations of the adhesion molecules. We conclude that volume therapy with hydroxyethyl starch resulted in a decrease in circulating adhesion molecules in our trauma patients. In contrast, volume therapy with albumin did not exert this effect. Continuous infusion of pentoxifylline did not have a beneficial modulating action on circulating adhesion molecules. PMID:8694202

Boldt, J; Heesen, M; Padberg, W; Martin, K; Hempelmann, G

1996-06-01

139

The production of chemotactic cytokines in an allogeneic response. The role of intercellular adhesion molecule-1 and lymphocyte function-associated antigen-3.  

PubMed Central

The in vitro mixed lymphocyte reaction (MLR) is regarded as a model of responsiveness to allogeneic major histocompatibility complex antigens and has historically been used to elucidate the pathway of T lymphocyte proliferation. In addition, the MLR response may reflect activation pathways relevant in acute allograft rejection. In the present study, we have applied the MLR to examine the role of adhesion molecules intercellular adhesion molecule-1 and lymphocyte function-associated antigen-3 in the induction of tumor necrosis factor-alpha (TNF-alpha) as well as chemotactic cytokines, interleukin-8 (IL-8), monocyte chemotactic protein-1 (MCP-1) and macrophage inflammatory protein-1 alpha (MIP-1 alpha). Monoclonal antibodies to the adhesion molecules (5 micrograms/ml) were added to one-way human MLR cultures and supernatants collected at various time points. The monoclonal antibodies to the adhesion molecules significantly suppressed the proliferative response by 50 to 80%. Cytokine production, TNF-alpha (3.2 +/- 0.5 ng/ml), MIP-1 alpha (12.9 +/- 3.3 ng/ml), MCP-1 (18.8 +/- 3.4 ng/ml), and IL-8 (57 +/- 18 ng/ml) peaked on day 5 of the assay. The addition of anti-intercellular adhesion molecule-1 to the cultures suppressed TNF-alpha, MIP-1 alpha, MCP-1, and IL-8 production by 68% (1.05 +/- 0.29 ng/ml), 85% (2.0 +/- 1.2 ng/ml), 63% (6.8 +/- 2.9 ng/ml), and 47% (30.3 +/- 3.7 ng/ml), respectively. Likewise, the addition of anti-lymphocyte function-associated antigen-3 monoclonal antibody suppressed the cytokines by 78% (0.71 +/- 0.34 ng/ml), 66% (4.5 +/- 2.2 ng/ml), 52% (8.8 +/- 2.2 ng/ml), and 73% (15.7 +/- 4.4 ng/ml), respectively. Immunohistochemical staining indicated that monocytes were the primary source of the chemokines IL-8, MCP-1, and MIP-1 alpha. The addition of exogenous recombinant TNF-alpha (5 ng/ml) or recombinant IL-2 (5 units/ml) to the anti-intercellular adhesion molecule-1-treated cultures allowed the recovery of the proliferative response as well as restoration of IL-2, TNF-alpha, and IL-8, but not MCP-1 or MIP-1 alpha, indicating that both soluble and adhesion molecule signals are required for the production of the C-C family of chemokines in allogeneic responses. Thus, the events resulting in cellular proliferation and chemokine production were dependent on adhesion molecule interactions. Images Figure 6

Lukacs, N. W.; Kunkel, S. L.; Burdick, M. D.; Strieter, R. M.

1993-01-01

140

Increased plasma and endothelial cell expression of chemokines and adhesion molecules in chronic kidney disease.  

PubMed

Chemokines and adhesion molecules are involved in early events of atherogenesis. In the present study, we investigated the effects of the uremic milieu on the expression of monocyte chemoattractant protein-1 (MCP-1), interleukin-8 (IL-8), soluble vascular adhesion molecule-1 (sVCAM-1) and soluble intercellular adhesion molecule-1 (sICAM-1) and their relationship to cardiovascular status. Plasma samples were obtained from patients in different stages of chronic kidney disease (CKD). Cardiovascular status was evaluated by intima-media thickness and endothelial dysfunction by flow mediation dilatation and proteinuria. In vitro studies were performed using human umbilical endothelial cells exposed to uremic plasma or plasma from healthy subjects. MCP-1, IL-8, sVCAM-1 and sICAM-1 levels in plasma and in supernatant were analyzed by enzyme-linked immunosorbent assay. The population consisted of 73 (mean age 57 years; 48% males) CKD patients with glomerular filtration rate (GFR) of 37 +/- 2 ml/min. MCP-1 and sVCAM-1 plasma levels were negatively correlated with GFR (rho = -0.40, p < 0.0005 and rho = -0.42, p < 0.0005, respectively). Fibrinogen was positively correlated with MCP-1, sICAM-1 and sVCAM-1 (rho = 0.33, p < 0.005, rho = 0.32, p < 0.05 and rho = 0.25, p < 0.05, respectively) and ultra-high-sensitivity C-reactive protein was positively correlated with sICAM-1 (rho = 0.25, p < 0.0005). Plasma IL-8 had a significant positive correlation with proteinuria (rho = 0.31, p < 0.01). There was a time- and CKD-stage-dependent MCP-1, IL-8 and sVCAM-1 endothelial expression (p < 0.05). In summary, plasma levels of markers of endothelial cell activation (MCP-1 and sVCAM-1) are increased in more advanced CKD. Exposure of endothelial cells to uremic plasma results in a time- and CKD-stage-dependent increased expression of MCP-1, IL-8 and sVCAM-1, suggesting a link between vascular activation, systemic inflammation and uremic toxicity. Future studies are necessary to investigate whether these biomarkers add predictive value in comparison to the previously described ones. Also, endothelial response to uremic toxicity should be viewed as a potential target for intervention in order to reduce morbidity and mortality in CKD-related cardiovascular disease. PMID:19147993

Stinghen, A E M; Gonçalves, S M; Martines, E G; Nakao, L S; Riella, M C; Aita, C A; Pecoits-Filho, R

2009-01-01

141

Increased expression of mucosal addressin cell adhesion molecule-1 (MAdCAM-1) and lymphocyte recruitment in murine gastritis induced by Helicobacter pylori  

PubMed Central

Although T cell involvement in Helicobactor pylori-induced gastritis is known, mechanism about T cell recruitment is not understood. In this study we examined how mucosal addressin cell adhesion molecule-1 (MAdCAM-1) is involved in lymphocyte recruitment in murine chronic gastritis induced by H. pylori. C57 BL/6 mice were infected with Sydney strain (SS1). Six months after infection, the stomach was removed. The expression of adhesion molecules, MAdCAM-1, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), and the cell surface antigens CD4, CD8, CD45R/B220 or ?7-integrin were determined by immunohistochemistry. A significant increase in CD4 lymphocytes was observed in the body portion of stomach in SS1-infected mice and most of these CD4 cells express ?7-integrin, a known counter ligand for MAdCAM-1 molecule. Strong MAdCAM-1 expression was observed adjacent to these cells in the lamina propria as well as in the submucosa of SS1-infected stomach. Quantitative analysis showed that the area of MAdCAM-1 expression well correlated with the infiltration of ?7-integrin positive lymphocytes. On the other hand, expression of ICAM-1 or VCAM-1 in the lamina propria was few even in the SS1-infected stomach. Increased expression of MAdCAM-1 was well correlated to the location of lymphocytes, which express CD4 and ?7-integrin. These results suggest the possibility that MAdCAM-1 may be largely involved in the lymphocyte recruitment in the gastritis mucosa with H. pylori.

Hatanaka, K; Hokari, R; Matsuzaki, K; Kato, S; Kawaguchi, A; Nagao, S; Suzuki, H; Miyazaki, K; Sekizuka, E; Nagata, H; Ishii, H; Miura, S

2002-01-01

142

Platelet endothelial cell adhesion molecule-1 modulates endothelial cell motility through the small G-protein Rho  

Microsoft Academic Search

Platelet endothelial cell adhesion mole- cule-1 (PECAM-1), an immunoglobulin family vascular adhesion molecule, is involved in endothelial cell mi- gration and angiogenesis (1, 2). We found that endo- thelial cells lacking PECAM-1 exhibit increased single cell motility and extension formation but poor wound healing migration, reminiscent of cells in which Rho activity has been suppressed by overexpressing a GTPase-activating protein

DITA GRATZINGER; SANDRA CANOSA; BRITTA ENGELHARDT; JOSEPH A. MADRI

2003-01-01

143

Inhibition of cytokine-induced vascular cell adhesion molecule-1 expression; possible mechanism for anti-atherogenic effect of Agastache rugosa.  

PubMed

Adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1) play an important role during the early stages of atherogenesis. Agastache rugosa has an anti-atherogenic effect in low density lipoprotein receptor -/- mice. Moreover, A. rugosa reduced macrophage infiltration and VCAM-1 expression has been localized in aortic endothelium that overlies early foam cell lesions. This study ascertained that tilianin (100 microM), a major component of A. rugosa, inhibits the tumor necrotic factor-alpha (TNF-alpha)-induced expression of VCAM-1 by 74% in cultured human umbilical vein endothelial cells (HUVECs). Also, tilianin (100 microM) reduced TNF-alpha-induced activation of nuclear factor-kappaB in HUVECs. PMID:11334881

Hong, J H; Choi, J H; Oh, S R; Lee, H K; Park, J H; Lee, K Y; Kim, J J; Jeong, T S; Oh, G T

2001-04-27

144

NOX2 in lung inflammation: quantum dot based in situ imaging of NOX2-mediated expression of vascular cell adhesion molecule-1.  

PubMed

Quantum dot (QD) imaging is a powerful tool for studying signaling pathways as they occur. Here we employ this tool to study adhesion molecule expression with lung inflammation in vivo. A key event in pulmonary inflammation is the regulation of vascular endothelial cell adhesion molecule-1 (VCAM), which drives activated immune cell adherence. The induction of VCAM expression is known to be associated with reactive oxygen species (ROS) production, but the exact mechanism or the cellular source of ROS that regulates VCAM in inflamed lungs is not known. NADPH oxidase 2 (NOX2) has been reported to be a major source of ROS with pulmonary inflammation. NOX2 is expressed by both endothelial and immune cells. Here we use VCAM-targeted QDs in a mouse model to show that NOX2, specifically endothelial NOX2, induces VCAM expression with lung inflammation in vivo. PMID:24318114

Orndorff, Rebecca L; Hong, Nankang; Yu, Kevin; Feinstein, Sheldon I; Zern, Blaine J; Fisher, Aron B; Muzykantov, Vladimir R; Chatterjee, Shampa

2014-02-01

145

Ganoderma lucidum polysaccharides attenuate endotoxin-induced intercellular cell adhesion molecule-1 expression in cultured smooth muscle cells and in the neointima in mice.  

PubMed

The expression of adhesion molecules on vessels and subsequent leukocyte recruitment are critical events in vascular diseases and inflammation. The aim of the present study was to examine the effects of an extract of Ganoderma lucidum (Reishi) polysaccharides (EORP), which is effective against cancer and immunological disorders, on adhesion molecule expression by human aortic smooth muscle cells (HASMCs) and the underlying mechanism. EORP significantly suppressed lipopolysaccharide (LPS)-induced intercellular cell adhesion molecule-1 (ICAM-1) mRNA and protein expression and reduced the binding of human monocytes to LPS-stimulated HASMCs. Immunoprecipitation and real-time polymerase chain reaction demonstrated that EORP markedly reduced the interaction of human antigen R protein (HuR) with the 3'-UTR of ICAM-1 mRNA in LPS-stimulated HASMCs. EORP treatment also suppressed extracellular signal-regulated kinase (ERK) phosphorylation and reduced the density of the shifted bands of nuclear factor (NF)-kappaB after LPS-induced activation. In an endothelial-denuded artery model in LPS-treated mice, daily oral administration of EORP for 2 weeks decreased neointimal hyperplasia and ICAM-1 expression in the plasma and neointima. These results provide evidence that EORP attenuates LPS-induced adhesion molecule expression and monocyte adherence and that this protective effect is mediated by decreased ERK phosphorylation and NF-kappaB activation. These findings suggest that EORP has anti-inflammatory properties and could prove useful in the prevention of vascular diseases and inflammatory responses. PMID:20687608

Lin, Ching-Yuang; Chen, Yung-Hsiang; Lin, Chia-Ying; Hsu, Hsien-Yeh; Wang, Shu-Huei; Liang, Chan-Jung; Kuan, I-I; Wu, Pei-Jhen; Pai, Pei-Ying; Wu, Chau-Chung; Chen, Yuh-Lien

2010-09-01

146

?d?2 Integrin Is Expressed on Human Eosinophils and Functions as an Alternative Ligand for Vascular Cell Adhesion Molecule 1 (VCAM-1)  

PubMed Central

The ?2 family of integrins, CD11a, CD11b, CD11c, and ?d, are expressed on most leukocytes. We show that the newest member of this family, ?d, is expressed on human eosinophils in peripheral blood, and surface expression can be upregulated within minutes by phorbol ester or calcium ionophore A23187. Culture of eosinophils with interleukin 5 (IL-5) leads to a two- to fourfold increase in ?d levels by 3–7 d without a change in ?4 integrin expression. Eosinophils isolated from late phase bronchoalveolar lavage fluids express ?d at levels similar to that seen after 3 d of IL-5 culture. Regarding ?d?2 ligands, in both freshly isolated and IL-5–cultured eosinophils, as well as ?d?2-transfected Chinese hamster ovary cells, ?d?2 can function as a ligand for vascular cell adhesion molecule 1 (VCAM-1). This conclusion is based on the ability of monoclonal antibodies to ?d, ?2, or VCAM-1 to block cell attachment in static adhesion assays. In experiments with eosinophils, the relative contribution of ?d?2 integrin– mediated adhesion is enhanced after IL-5 culture. These experiments demonstrate that ?d?2 is an alternative ligand for VCAM-1, and this integrin may play a role in eosinophil adhesion to VCAM-1 in states of chronic inflammation.

Grayson, Mitchell H.; Van der Vieren, Monica; Sterbinsky, Sherry A.; Michael Gallatin, W.; Hoffman, Patricia A.; Staunton, Donald E.; Bochner, Bruce S.

1998-01-01

147

Vascular cell adhesion molecule-1 (VCAM-1) gene transcription and expression are regulated through an antioxidant-sensitive mechanism in human vascular endothelial cells.  

PubMed Central

Oxidative stress and expression of the vascular cell adhesion molecule-1 (VCAM-1) on vascular endothelial cells are early features in the pathogenesis of atherosclerosis and other inflammatory diseases. Regulation of VCAM-1 gene expression may be coupled to oxidative stress through specific reduction-oxidation (redox) sensitive transcriptional or posttranscriptional regulatory factors. In cultured human umbilical vein endothelial (HUVE) cells, the cytokine interleukin 1 beta (IL-1 beta) activated VCAM-1 gene expression through a mechanism that was repressed approximately 90% by the antioxidants pyrrolidine dithiocarbamate (PDTC) and N-acetylcysteine (NAC). Furthermore, PDTC selectively inhibited the induction of VCAM-1, but not intercellular adhesion molecule-1 (ICAM-1), mRNA and protein accumulation by the cytokine tumor necrosis factor-alpha (TNF alpha) as well as the noncytokines bacterial endotoxin lipopolysaccharide (LPS) and double-stranded RNA, poly(I:C) (PIC). PDTC also markedly attenuated TNF alpha induction of VCAM-1-mediated cellular adhesion. In a distinct pattern, PDTC partially inhibited E-selectin gene expression in response to TNF alpha but not to LPS, IL-1 beta, or PIC. TNF alpha and LPS-mediated transcriptional activation of the human VCAM-1 promoter through NF-kappa B-like DNA enhancer elements and associated NF-kappa B-like DNA binding proteins was inhibited by PDTC. These studies suggest a molecular linkage between an antioxidant sensitive transcriptional regulatory mechanism and VCAM-1 gene expression that expands on the notion of oxidative stress as an important regulatory signal in the pathogenesis of atherosclerosis. Images

Marui, N; Offermann, M K; Swerlick, R; Kunsch, C; Rosen, C A; Ahmad, M; Alexander, R W; Medford, R M

1993-01-01

148

Inhibitory effect of indigo naturalis on tumor necrosis factor-?-induced vascular cell adhesion molecule-1 expression in human umbilical vein endothelial cells.  

PubMed

The use of indigo naturalis to treat psoriasis has proved effective in our previous clinical studies. The present study was designed to examine the anti-inflammatory effect of indigo naturalis in primary cultured human umbilical vein endothelial cells (HUVECs). Pretreatment of cells with indigo naturalis extract attenuated TNF-?-induced increase in Jurkat T cell adhesion to HUVECs as well as decreased the protein and messenger (m)RNA expression levels of vascular cell adhesion molecule-1 (VCAM-1) on HUVECs. Indigo naturalis extract also inhibited the protein expression of activator protein-1 (AP-1)/c-Jun, a critical transcription factor for the activation of VCAM-1 gene expression. Since the reduction of lymphocyte adhesion to vascular cells by indigo naturalis extract could subsequently reduce the inflammatory reactions caused by lymphocyte infiltration in the epidermal layer and help to improve psoriasis, this study provides a potential mechanism for the anti-inflammatory therapeutic effect of indigo naturalis extract in psoriasis. PMID:20877233

Chang, Hsin-Ning; Pang, Jong-Hwei Su; Yang, Sien-Hung; Hung, Chi-Feng; Chiang, Chi-Hsin; Lin, Tung-Yi; Lin, Yin-Ku

2010-09-01

149

Dileucine and PDZ-binding Motifs Mediate Synaptic Adhesion-like Molecule 1 (SALM1) Trafficking in Hippocampal Neurons*  

PubMed Central

Synaptic adhesion-like molecules (SALMs) are a family of cell adhesion molecules involved in neurite outgrowth and synapse formation. Of the five family members, only SALM1, -2, and -3 contain a cytoplasmic C-terminal PDZ-binding motif. We have found that SALM1 is unique among the SALMs because deletion of its PDZ-binding motif (SALM1?PDZ) blocks its surface expression in heterologous cells. When expressed in hippocampal neurons, SALM1?PDZ had decreased surface expression in dendrites and the cell soma but not in axons, suggesting that the PDZ-binding domain may influence cellular trafficking of SALMs to specific neuronal locations. Endoglycosidase H digestion assays indicated that SALM1?PDZ is retained in the endoplasmic reticulum (ER) in heterologous cells. However, when the entire C-terminal tail of SALM1 was deleted, SALM1 was detected on the cell surface. Using serial deletions, we identified a region of SALM1 that contains a putative dileucine ER retention motif, which is not present in the other SALMs. Mutation of this DXXXLL motif allowed SALM1 to leave the ER and enhanced its surface expression in heterologous cells and neurons. An increase in the number of protrusions at the dendrites and cell body was observed when this SALM1 mutant was expressed in hippocampal neurons. With electron microscopy, these protrusions appeared to be irregular, enlarged spines and filopodia. Thus, enrichment of SALM1 on the cell surface affects dendritic arborization, and intracellular motifs regulate its dendritic versus axonal localization.

Seabold, Gail K.; Wang, Philip Y.; Petralia, Ronald S.; Chang, Kai; Zhou, Arthur; McDermott, Mark I.; Wang, Ya-Xian; Milgram, Sharon L.; Wenthold, Robert J.

2012-01-01

150

Amino Acid Sequences Mediating Vascular Cell Adhesion Molecule 1 Binding to Integrin Alpha 4: Homologous DSP Sequence Found for JC Polyoma VP1 Coat Protein.  

PubMed

The JC polyoma viral coat protein VP1 was analyzed for amino acid sequences homologies to the IDSP sequence which mediates binding of VLA-4 (integrin alpha 4) to vascular cell adhesion molecule 1. Although the full sequence was not found, a DSP sequence was located near the critical arginine residue linked to infectivity of the virus and binding to sialic acid containing molecules such as integrins (3). For the JC polyoma virus, a DSP sequence was found at residues 70, 71 and 72 with homology also noted for the mouse polyoma virus and SV40 virus. Three dimensional modeling of the VP1 molecule suggests that the DSP loop has an accessible site for interaction from the external side of the assembled viral capsid pentamer. PMID:24147211

Meyer, Michael Andrew

2013-01-01

151

Role of isoprenylcysteine carboxyl methyltransferase in tumor necrosis factor-alpha stimulation of expression of vascular cell adhesion molecule-1 in endothelial cells.  

PubMed

We have previously shown that cytokine stimulation of the expression of vascular cell adhesion molecule-1 (VCAM-1), but not that of intercellular adhesion molecule-1 (ICAM-1), is redox sensitive in endothelial cells. Here, we investigated the role of isoprenylcysteine carboxyl methyltransferase (ICMTase), which methylates isoprenylated CAAX (where C indicates cysteine; A, aliphatic amino acids; and X, almost any other amino acid) proteins, including Rac1, a component of superoxide-generating NAD(P)H oxidase, in the expression of VCAM-1. Pretreatment of endothelial cells with N-acetyl-S-farnesyl-L-cysteine (AFC) or N-acetyl-S-geranylgeranyl-L-cysteine (AGGC), specific inhibitors of ICMTase, inhibited the tumor necrosis factor-alpha (TNF-alpha) stimulation of mRNA expression of VCAM-1 but not that of ICAM-1. Endothelial cells expressed constitutively active ICMTase, as suggested by the presence of methylated Rac1 and the methylation of AFC by the cells. TNF-alpha stimulation of the cells significantly increased the methylation of AFC and Rac1 in endothelial cells. That ICMTase was a component of the redox-sensitive signaling pathway was also suggested by the AFC inhibition of the generation of reactive oxygen species by TNF-alpha. Interestingly, the dominant-negative isoform of Rac1 was not selective but inhibited the TNF-alpha stimulation of the mRNA expression of VCAM-1 and ICAM-1. Thus, ICMTase is a critical component of the redox-sensitive VCAM-1-selective signaling pathway, and it appears to activate a discrete inflammatory signaling pathway, at least in part, through the methylation of Rac1. PMID:12006387

Ahmad, Mushtaq; Zhang, Yan; Zhang, Yong; Papharalambus, Christopher; Alexander, R Wayne

2002-05-01

152

Intercellular adhesion molecule 1/2 and E-selectin in plasma cell mastitis: immunohistochemical study of 35 cases.  

PubMed

Plasma cell mastitis (PCM) is one of the most frequently encountered inflammatory diseases of the nonlactating breast. Histologically, PCM is characterized by infiltration of relatively abundant plasma cells into the mammary ducts. Its pathogenesis has remained unknown. In this study, we immunolocalized intercellular adhesion molecule (ICAM) 1 and 2 and E-selectin, all of which play pivotal roles in the inflammatory process, in 35 cases of PCM. We then compared the results with those of non-PCM and nonpathologic breast tissue. In the ductal epithelium, ICAM-1 immunoreactivity was significantly more pronounced in PCM than in non-PCM (P = .045). Both ICAM-1 (P < .001) and ICAM-2 (P = .001) were significantly more pronounced in PCM than in nonpathologic breast tissue. However, no significant differences in ICAM-2 and E-selectin immunoreactivity were detected between ductal epithelium of PCM and non-PCM. ICAM-1, but not ICAM-2 or E-selectin, demonstrated significantly higher immunoreactivity in endothelial cells of PCM than in nonpathologic breast (P < .001). These results all suggest that ICAM-1 in both ductal epithelium and endothelium plays important roles in the inflammatory process of PCM, possibly through margination, extravasation, and attachment of plasma cells and lymphocytes, which may result in continuous inflammatory cell homing to ductal epithelial cells. PMID:24457076

Dong, Yu; Yu, Jian-Jun; Shibahara, Yukiko; Lu, Huai-Sheng; He, Hai-Yan; Liu, Jian-Dong; Chen, Shi-Fan; Wang, Lin; Zhang, Ye; Felizola, Saulo J A; Chan, Monica S M; Ono, Katsuhiko; Ishida, Takanori; Ohuchi, Noriaki; Sasano, Hironobu

2014-03-01

153

Monocyte trafficking to hepatic sites of bacterial infection is chemokine independent and directed by focal intercellular adhesion molecule-1 expression.  

PubMed

Recruitment of CCR2(+)Ly6C(high) monocytes to sites of infection is essential for efficient clearance of microbial pathogens. Although CCR2-mediated signals promote monocyte emigration from bone marrow, the contribution of CCR2 to later stages of monocyte recruitment remains unresolved. In this article, we show that CCR2 deficiency markedly worsens hepatic Listeria monocytogenes infection because Ly6C(high) monocytes are retained in the bone marrow. Intravenously transferred, CCR2-deficient Ly6C(high) monocytes traffic normally to hepatic foci of infection and contribute to bacterial clearance. Pertussis toxin treatment of adoptively transferred monocytes does not impair their intrahepatic trafficking, suggesting that chemokine signaling, once CCR2(+)Ly6C(high) monocytes emigrate from the bone marrow, is not required for monocyte localization to sites of bacterial infection in the liver. Expression of ICAM-1 is induced in close proximity to foci of bacterial infection in the liver, including on CD31(+) endothelial cells, and blockade of CD11b and CD44 diminishes monocyte localization to these hepatic foci. Our studies demonstrated that Ly6C(high) monocyte recruitment from the bloodstream to the L. monocytogenes-infected liver does not require chemokine receptor-mediated signals but instead is principally dependent on integrin- and extracellular matrix-mediated monocyte adhesion. PMID:20435926

Shi, Chao; Velázquez, Peter; Hohl, Tobias M; Leiner, Ingrid; Dustin, Michael L; Pamer, Eric G

2010-06-01

154

The Integrin a 9 b 1 Mediates Adhesion to Activated Endothelial Cells and Transendothelial Neutrophil Migration through Interaction with Vascular Cell Adhesion Molecule1  

Microsoft Academic Search

The integrin a 9 b 1 has been shown to be widely expressed on smooth muscle and epithelial cells, and to mediate adhesion to the extracellular matrix proteins osteopontin and tenascin-C. We have found that the peptide sequence this integrin recognizes in tenascin-C is highly homologous to the sequence recog- nized by the closely related integrin a 4 b 1,

Yasuyuki Taooka; John Chen; Ted Yednock; Dean Sheppard

155

Hydrogen peroxide mediates vascular cell adhesion molecule-1 expression from interleukin-18-activated hepatic sinusoidal endothelium: implications for circulating cancer cell arrest in the murine liver.  

PubMed

The mechanism of intrasinusoidal arrest of circulating cancer cells, which is a critical step in liver metastasis, appears to be facilitated by tumor-derived proinflammatory factors that increase sinusoidal cell adhesion receptors for cancer cells. However, how this prometastatic microenvironment is up-regulated remains unknown. Using intrasplenically injected B16 melanoma (B16M) cells, we show that the expression of vascular cell adhesion molecule-1 (VCAM-1) significantly increased in hepatic sinusoidal endothelium (HSE) cells over physiologic baseline within the first 24 hours of metastatic cancer cell infiltration in the liver. This correlated with increased in vitro adhesion of B16M cells to HSE cells isolated from B16M cell-injected mice. In vivo VCAM-1 blockade with specific antibodies before B16M cell injection decreased sinusoidal retention of luciferase-transfected B16M cells by 85%, and metastasis development by 75%, indicating that VCAM-1 expression on tumor-activated HSE cells had a prometastatic contribution. Because VCAM-1 expression is oxidative stress-inducible, recombinant catalase was in vivo administered, resulting in a complete abrogation of both VCAM-1 expression and B16M cell adhesion increases in HSE cells isolated from B16M cell-injected mice. Catalase also abrogated the proadhesive response of HSE cells to B16M-conditioned medium (B16M-CM) in vitro, although this did not affect the concomitant release of major proinflammatory cytokines by HSE cells. HSE cells treated with B16M-CM released interleukin (IL)-18 via tumor necrosis factor-alpha (TNF-alpha)-dependent IL-1beta in vitro. In turn, H(2)O(2) production from B16M-CM-treated HSE cells was regulated by IL-18. Thus, liver-infiltrating B16M cells activated their adhesion to HSE through a sequential process involving TNF-alpha-dependent IL-1beta, which induced IL-18 to up-regulate VCAM-1 via H(2)O(2). The pivotal position of H(2)O(2) was further supported by the fact that incubation of HSE cells with nontoxic concentrations of H(2)O(2) directly enhanced VCAM-1-dependent B16M cell adhesion in vitro without proinflammatory cytokine mediation, which emphasizes the key role of oxidative stress in the pathogenesis of liver inflammation and metastasis. PMID:11481615

Mendoza, L; Carrascal, T; De Luca, M; Fuentes, A M; Salado, C; Blanco, J; Vidal-Vanaclocha, F

2001-08-01

156

Transcriptional activation of the vascular cell adhesion molecule-1 gene in T lymphocytes expressing human T-cell leukemia virus type 1 Tax protein.  

PubMed Central

Recruitment and extravasation of T cells through the blood-brain barrier are favored by adhesion molecule-mediated interactions of circulating T cells with endothelial cells. Since a common pathological finding in human T-cell leukemia virus type 1 (HTLV-1)-associated diseases is the infiltration of HTLV-1-infected T lymphocytes into various organs, we have looked for the profile of adhesion molecules expressed by HTLV-1-transformed T cells. Flow cytometry analysis indicated that these cells were expressing high levels of vascular cell adhesion molecule 1 (VCAM-1 [CD106]), a 110-kDa member of the immunoglobulin gene superfamily, first identified on endothelial cells stimulated with inflammatory cytokines. This adhesion molecule was also expressed by T cells obtained from one patient with HTLV-1-associated myelopathy/tropical spastic paraparesis but not by activated T cells isolated from one normal blood donor. The role of the viral trans-activator Tax protein in the induction of VCAM-1 was first indicated by the detection of this adhesion molecule on Jurkat T-cell clones stably expressing the tax gene. The effect of Tax on VCAM-1 gene transcription was next confirmed in JPX-9 cells, a subclone of Jurkat cells, carrying the tax sequences under the control of an inducible promoter. Furthermore, deletion and mutation analyses of the VCAM-1 promoter performed with chloramphenicol acetyltransferase constructs revealed that Tax was trans activating the VCAM-1 promoter via two NF-kappaB sites present at bp -72 and -57 in the VCAM-1 gene promoter, with both of them being required for the Tax-induced expression of this adhesion molecule. Finally, gel mobility shift assays demonstrated the nuclear translocation of proteins specifically bound to these two NF-kappaB motifs, confirming that VCAM-1 was induced on Tax-expressing cells in a kappaB-dependent manner. Collectively, these results therefore suggest that the exclusive Tax-induced expression of VCAM-1 on T cells may represent a pivotal event in the progression of HTLV-1-associated diseases.

Valentin, H; Lemasson, I; Hamaia, S; Casse, H; Konig, S; Devaux, C; Gazzolo, L

1997-01-01

157

Calcium mobilization and Rac1 activation are required for VCAM-1 (vascular cell adhesion molecule-1) stimulation of NADPH oxidase activity.  

PubMed Central

VCAM-1 (vascular cell adhesion molecule-1) plays an important role in the regulation of inflammation in atherosclerosis, asthma, inflammatory bowel disease and transplantation. VCAM-1 activates endothelial cell NADPH oxidase, and this oxidase activity is required for VCAM-1-dependent lymphocyte migration. We reported previously that a mouse microvascular endothelial cell line promotes lymphocyte migration that is dependent on VCAM-1, but not on other known adhesion molecules. Here we have investigated the signalling mechanisms underlying VCAM-1 function. Lymphocyte binding to VCAM-1 on the endothelial cell surface activated an endothelial cell calcium flux that could be inhibited with anti-alpha4-integrin and mimicked by anti-VCAM-1-coated beads. VCAM-1 stimulation of calcium responses could be blocked by an inhibitor of intracellular calcium mobilization, a calcium channel inhibitor or a calcium chelator, resulting in the inhibition of NADPH oxidase activity. Addition of ionomycin overcame the calcium channel blocker suppression of VCAM-1-stimulated NADPH oxidase activity, but could not reverse the inhibitory effect imposed by intracellular calcium blockage, indicating that both intracellular and extracellular calcium mobilization are required for VCAM-1-mediated activation of NADPH oxidase. Furthermore, VCAM-1 specifically activated the Rho-family GTPase Rac1, and VCAM-1 activation of NADPH oxidase was blocked by a dominant negative Rac1. Thus VCAM-1 stimulates the mobilization of intracellular and extracellular calcium and Rac1 activity that are required for the activation of NADPH oxidase.

Cook-Mills, Joan M; Johnson, Jacob D; Deem, Tracy L; Ochi, Atsuo; Wang, Lei; Zheng, Yi

2004-01-01

158

FRET Based Quantification and Screening Technology Platform for the Interactions of Leukocyte Function-Associated Antigen-1 (LFA-1) with InterCellular Adhesion Molecule-1 (ICAM-1)  

PubMed Central

The interaction between leukocyte function-associated antigen-1(LFA-1) and intercellular adhesion molecule-1 (ICAM-1) plays a pivotal role in cellular adhesion including the extravasation and inflammatory response of leukocytes, and also in the formation of immunological synapse. However, irregular expressions of LFA-1 or ICAM-1 or both may lead to autoimmune diseases, metastasis cancer, etc. Thus, the LFA-1/ICAM-1 interaction may serve as a potential therapeutic target for the treatment of these diseases. Here, we developed one simple ‘in solution’ steady state fluorescence resonance energy transfer (FRET) technique to obtain the dissociation constant (Kd) of the interaction between LFA-1 and ICAM-1. Moreover, we developed the assay into a screening platform to identify peptides and small molecules that inhibit the LFA-1/ICAM-1 interaction. For the FRET pair, we used Alexa Fluor 488-LFA-1 conjugate as donor and Alexa Fluor 555-human recombinant ICAM-1 (D1-D2-Fc) as acceptor. From our quantitative FRET analysis, the Kd between LFA-1 and D1-D2-Fc was determined to be 17.93±1.34 nM. Both the Kd determination and screening assay were performed in a 96-well plate platform, providing the opportunity to develop it into a high-throughput assay. This is the first reported work which applies FRET based technique to determine Kd as well as classifying inhibitors of the LFA-1/ICAM-1 interaction.

Chakraborty, Sandeep; Nunez, David; Hu, Shih-Yang; Domingo, Maria Pilar; Pardo, Julian; Karmenyan, Artashes; Chiou, Arthur

2014-01-01

159

Modified low density lipoprotein and its constituents augment cytokine-activated vascular cell adhesion molecule-1 gene expression in human vascular endothelial cells.  

PubMed Central

Early features in the pathogenesis of atherosclerosis include accumulation of oxidized LDL (oxLDL) and endothelial expression of the vascular adhesion molecule VCAM-1. Because antioxidants inhibit endothelial VCAM-1 expression, we tested the hypothesis that oxLDL functions as a prooxidant signal in atherogenesis to augment VCAM-1 activation by inflammatory signals. Cultured human aortic endothelial cells (HAECs) or human umbilical vein endothelial cells (HUVECs) were incubated with unmodified LDL, oxLDL, or glycated LDL for 48 h. No change in VCAM-1, intercellular cell adhesion molecule-1 (ICAM-1), or E-selectin expression from control was observed by ELISA. However, dose-response and time course studies demonstrated that oxLDL enhanced VCAM-1 expression induced by the cytokin tumor necrosis factor alpha (TNF alpha) 63% in HAECs and 45% in HUVECs over unmodified LDL or control. Using flow cytometry analysis, oxLDL augmented TNF alpha-induced VCAM-1 expression in a uniform HAEC population. oxLDL had no effect on E-selection induction. oxLDL augmented TNF alpha-induced ICAM-1 expression 44% in HAECs but not in HUVECs. Glycated LDL augmented TNF alpha-induced VCAM-1 expression 35% in HAECs but not HUVECs. Similar results were obtained with 13-HPODE or lysophosphatidylcholine, significant components of oxLDL. 13-HPODE augmented TNF alpha-induced mRNA accumulation and transcriptional activation of VCAM-1 in HAECs. These results suggest that as long-term regulatory signals, specific oxidized fatty acid and phospholipid components of oxLDL augment the ability of vascular endothelial cells to express cytokine-mediated VCAM-1. These studies link oxidant signals conferred by oxLDL to oxidation-sensitive regulatory mechanisms controlling the expression of endothelial cell adhesion molecules involved in early atherosclerosis. Images

Khan, B V; Parthasarathy, S S; Alexander, R W; Medford, R M

1995-01-01

160

Modified low density lipoprotein and its constituents augment cytokine-activated vascular cell adhesion molecule-1 gene expression in human vascular endothelial cells.  

PubMed

Early features in the pathogenesis of atherosclerosis include accumulation of oxidized LDL (oxLDL) and endothelial expression of the vascular adhesion molecule VCAM-1. Because antioxidants inhibit endothelial VCAM-1 expression, we tested the hypothesis that oxLDL functions as a prooxidant signal in atherogenesis to augment VCAM-1 activation by inflammatory signals. Cultured human aortic endothelial cells (HAECs) or human umbilical vein endothelial cells (HUVECs) were incubated with unmodified LDL, oxLDL, or glycated LDL for 48 h. No change in VCAM-1, intercellular cell adhesion molecule-1 (ICAM-1), or E-selectin expression from control was observed by ELISA. However, dose-response and time course studies demonstrated that oxLDL enhanced VCAM-1 expression induced by the cytokin tumor necrosis factor alpha (TNF alpha) 63% in HAECs and 45% in HUVECs over unmodified LDL or control. Using flow cytometry analysis, oxLDL augmented TNF alpha-induced VCAM-1 expression in a uniform HAEC population. oxLDL had no effect on E-selection induction. oxLDL augmented TNF alpha-induced ICAM-1 expression 44% in HAECs but not in HUVECs. Glycated LDL augmented TNF alpha-induced VCAM-1 expression 35% in HAECs but not HUVECs. Similar results were obtained with 13-HPODE or lysophosphatidylcholine, significant components of oxLDL. 13-HPODE augmented TNF alpha-induced mRNA accumulation and transcriptional activation of VCAM-1 in HAECs. These results suggest that as long-term regulatory signals, specific oxidized fatty acid and phospholipid components of oxLDL augment the ability of vascular endothelial cells to express cytokine-mediated VCAM-1. These studies link oxidant signals conferred by oxLDL to oxidation-sensitive regulatory mechanisms controlling the expression of endothelial cell adhesion molecules involved in early atherosclerosis. PMID:7533787

Khan, B V; Parthasarathy, S S; Alexander, R W; Medford, R M

1995-03-01

161

Recruitment of lymphocytes during cutaneous delayed hypersensitivity in nonhuman primates is dependent on E-selectin and vascular cell adhesion molecule 1.  

PubMed Central

Previous investigations of cutaneous delayed hypersensitivity (DHR) in humans and animals have demonstrated that lymphocyte recruitment from blood is temporally and spatially associated with the de novo, asynchronous expression of both vascular cell adhesion molecule 1 (VCAM-1) and E-selectin on dermal endothelium. In this study, DHR was induced in rhesus monkeys sensitized against tuberculin in order to investigate the contribution of E-selectin and VCAM-1 in lymphocyte recruitment to skin. Intravenous infusions of neutralizing doses of F(ab')2 fragments of murine antibodies to either E-selectin or VCAM-1 during the early inductive phases of DHR showed that murine IgG localized to dermal endothelium at the site of DHR in a pattern kinetically similar to the expression of each endothelial adhesion protein. Most importantly, the relative numbers of lymphocytes localized to the inflammatory site were significantly reduced in DHR modified with infusions of antibodies to either VCAM-1 or E-selectin, while the numbers of lymphocytes recruited to skin in the animal given F(ab')2 fragments of an irrelevant murine monoclonal antibody of the same isotype and at the same dose were not changed. Moreover, in individual animals, the relative inhibition achieved with a particular antibody was proportional to the magnitude of expression of the targeted adhesion protein. Therefore, both VCAM-1 and E-selectin are functionally relevant in the genesis of cutaneous DHR, and each appears to contribute to lymphocyte recruitment in relation to its relative degree of expression in any one particular animal. Images

Silber, A; Newman, W; Sasseville, V G; Pauley, D; Beall, D; Walsh, D G; Ringler, D J

1994-01-01

162

GroEL1, from Chlamydia pneumoniae, Induces Vascular Adhesion Molecule 1 Expression by p37AUF1 in Endothelial Cells and Hypercholesterolemic Rabbit  

PubMed Central

The expression of vascular adhesion molecule-1 (VCAM-1) by endothelial cells may play a major role in atherogenesis. The actual mechanisms of chlamydia pneumoniae (C. pneumoniae) relate to atherogenesis are unclear. We investigate the influence of VCAM-1 expression in the GroEL1 from C. pneumoniae-administered human coronary artery endothelial cells (HCAECs) and hypercholesterolemic rabbits. In this study, we constructed the recombinant GroEL1 from C. pneumoniae. The HCAECs/THP-1 adhesion assay, tube formation assay, western blotting, enzyme-linked immunosorbent assay, actinomycin D chase experiment, luciferase reporter assay, and immunohistochemical stainings were performed. The results show that GroEL1 increased both VCAM-1expression and THP-1 cell adhesives, and impaired tube-formation capacity in the HCAECs. GroEL1 significantly increased the VCAM-1 mRNA stability and cytosolic AU-binding factor 1 (AUF1) level. Overexpression of the p37AUF1 significantly increased VCAM-1 gene expression in GroEL1-induced bovine aortic endothelial cells (BAECs). GroEL1 prolonged the stability of VCAM-1 mRNA by increasing both p37AUF1 and the regulation of the 5? untranslated region (UTR) of the VCAM-1 mRNA in BAECs. In hypercholesterolemic rabbits, GroEL1 administration enhanced fatty-streak and macrophage infiltration in atherosclerotic lesions, which may be mediated by elevated VCAM-1 expression. In conclusion, GroEL1 induces VCAM-1 expression by p37AUF1 in endothelial cells and enhances atherogenesis in hypercholesterolemic rabbits.

Shih, Chun-Ming; Tsao, Nai-Wen; Chen, Yung-Hsiang; Li, Chi-Yuan; Chang, Yu-Jia; Chang, Nen-Chung; Ou, Keng-Liang; Lin, Cheng-Yen; Nien, Chih-Hao; Lin, Feng-Yen

2012-01-01

163

A Fibrinogen-Derived Peptide Provides Intercellular Adhesion Molecule-1-Specific Targeting and Intraendothelial Transport of Polymer Nanocarriers in Human Cell Cultures and Mice  

PubMed Central

Intercellular adhesion molecule-1 (ICAM-1), a transmembrane glycoprotein expressed on activated endothelium and many other cells, represents a suitable target for delivery of drug nanocarriers (NCs) to disease areas. Numerous works have shown efficient targeting and intracellular transport of ICAM-1-targeted NCs, rendering significant therapeutic potential. This is the case for enzyme delivery for treatment of multitissue lysosomal storage disorders. However, those studies used formulations targeted to ICAM-1 by antibodies (anti-ICAM NCs). This poses an obstacle to preclinical evaluation of long-term treatment of such chronic maladies, caused by immunogenicity of foreign proteins administered to animals, compelling development of alternative strategies. In this work, we used radioisotope tracing, fluorescence and electron microscopy, and in vitro, cell cultures, and mouse models to evaluate polymer nanocarriers targeted to ICAM-1 by a 17-mer linear peptide derived from the ICAM-1-binding sequence of fibrinogen (?3). Our results show that ?3 NCs target ICAM-1 with efficiency and specificity similar to that of anti-ICAM NCs, determined by using immobilized ICAM-1, native ICAM-1 expressed on endothelial cell cultures, and intravenous administration in mice. Furthermore, ?3 NCs are internalized by cells in culture and in vivo and transported to lysosomes via cell adhesion molecule-mediated endocytosis, without apparent disruption of cell junctions, similar to anti-ICAM counterparts. The degree of conservation of fibrinogen ?3 sequence and its cognate site on ICAM-1 among species (e.g., mouse, chimpanzee, and humans) reflects the interspecies targeting found for ?3 NCs, providing an avenue for exploring the translation of ICAM-1-targeting platforms in the preclinical and, perhaps, future clinical realm.

Garnacho, Carmen; Serrano, Daniel

2012-01-01

164

Molecular cloning of a cell-surface glycoprotein that can potentially discriminate mesothelium from epithelium: its identification as vascular cell adhesion molecule 1.  

PubMed Central

It has long been a practical problem for surgical pathologists to distinguish mesothelium from epithelium in order to make a positive diagnosis of mesothelioma. In this study, we developed a new monoclonal antibody, designated MS-2761 (IgG1, k), against cultured non-neoplastic mesothelial cells. Immunohistochemistry and slot-blot analysis revealed that this monoclonal antibody reacted with 100% (12/12) of benign and malignant mesothelioma tissues and a mesothelioma cell line, but not with 99% (77/78) of epithelial tumour tissues and 97% (33/34) of epithelial tumour cell lines. A gene encoding the cell-surface antigen defined by this monoclonal antibody was isolated from a mesothelial cell cDNA library constructed with a mammalian cell expression vector through transfection of Cos-7 cells and immunoselection by panning. DNA sequencing and a database search revealed that the gene was identical to vascular cell adhesion molecule 1 (VCAM1, also referred to as INCAM110). The prominent VCAM1 transcript in mesothelium was 3.2 kb in size with seven Ig-like domains, in addition to a minor transcripts with six Ig-like domains. This monoclonal antibody potentially discriminates mesothelium from epithelium and may become a tool for differential diagnosis of mesothelioma. Images Figure 1 Figure 2 Figure 3 Figure 4 Figure 6 Figure 7

Yamada, T.; Jiping, J.; Endo, R.; Gotoh, M.; Shimosato, Y.; Hirohashi, S.

1995-01-01

165

Cocaine-associated retiform purpura: a C5b-9-mediated microangiopathy syndrome associated with enhanced apoptosis and high levels of intercellular adhesion molecule-1 expression.  

PubMed

Cocaine-associated retiform purpura is a recently described entity characterized by striking hemorrhagic necrosis involving areas of skin associated with administration of cocaine. Levamisole, an adulterant in cocaine, has been suggested as the main culprit pathogenetically. Four cases of cocaine-associated retiform purpura were encountered in the dermatopathology practice of C. M. Magro. The light microscopic findings were correlated with immunohistochemical and immunofluorescence studies. All 4 cases showed a very striking thrombotic diathesis associated with intravascular macrophage accumulation. Necrotizing vasculitis was noted in 1 case. Striking intercellular adhesion molecule-1 (ICAM-1)/CD54 expression in vessel wall along with endothelial expression of caspase 3 and extensive vascular C5b-9 deposition was observed in all biopsies examined. Cocaine-induced retiform purpura is a C5b-9-mediated microvascular injury associated with enhanced apoptosis and prominent vascular expression of ICAM-1, all of which have been shown in prior in vitro and in vivo murine models to be a direct effect of cocaine metabolic products. Antineutrophilic cytoplasmic antibody and antiphospholipid antibodies are likely the direct sequelae of the proapoptotic microenvironment. The inflammatory vasculitic lesion could reflect the downstream end point reflective of enhanced ICAM-1 expression and the development of antineutrophilic cytoplasmic antibody. Levamisole likely works synergistically with cocaine in the propagation of this syndromic complex. PMID:23392134

Magro, Cynthia M; Wang, Xuan

2013-10-01

166

Prostaglandin E2-induced intercellular adhesion molecule-1 expression is mediated by cAMP/Epac signalling modules in bEnd.3 brain endothelial cells  

PubMed Central

Background and Purpose Prostaglandin E2 (PGE2) has been implicated in the regulation of adhesion molecules, leukocyte adhesion and infiltration into inflamed site. However, the underlying mechanism therein involved remains ill-defined. In this study, we explored its cellular mechanism of action in the regulation of the intercellular adhesion molecule-1 (ICAM-1) expression in the brain endothelial cells. Experimental Approach bEnd.3 cells, the murine cerebrovascular endothelial cell line and primary mouse brain endothelial cells were treated with PGE2 with or without agonists/antagonists of PGE2 receptors and associated signalling molecules. ICAM-1 expression, Akt phosphorylation and activity of NF-?B were determined by reverse transcription polymerase chain reaction (RT-PCR), immunoblot analysis, luciferase assay and immunocytochemistry. Key Results PGE2 significantly up-regulated the expression of ICAM-1, which was blocked by EP4 antagonist (ONO-AE2-227) and knock-down of EP4. PGE2 effects were mimicked by forskolin, dibutyryl cAMP (dbcAMP) and an exchange protein directly activated by cAMP (Epac) activator (8-Cpt-cAMP) but not a protein kinase A activator (N6-Bnz-cAMP). PGE2-induced ICAM-1 expression was reduced by knock-down of Epac1. A PI3K specific inhibitor (LY294002), Akt inhibitor VIII (Akti) and NF-?B inhibitors (Bay-11–7082 and MG-132) attenuated the induction of ICAM-1 by PGE2. PGE2, dbcAMP and 8-Cpt-cAMP induced the phosphorylation of Akt, I?B kinase and I?B? and the translocation of p65 to the nucleus and increased NF-?B dependent reporter gene activity, which was diminished by Akti. Conclusion and Implications Our findings suggest that PGE2 induces ICAM-1 expression via EP4 receptor and Epac/Akt/NF-?B signalling pathway in bEnd.3 brain endothelial cells, supporting its pathophysiological role in brain inflammation.

Park, Tae Yeop; Baik, Eun Joo; Lee, Soo Hwan

2013-01-01

167

Levels of soluble endothelium-derived adhesion molecules in patients with sickle cell disease are associated with pulmonary hypertension, organ dysfunction, and mortality  

PubMed Central

Summary Endothelial cell adhesion molecules orchestrate the recruitment and binding of inflammatory cells to vascular endothelium. With endothelial dysfunction and vascular injury, the levels of endothelial bound and soluble adhesion molecules increase. Such expression is modulated by nitric oxide (NO), and in patients with sickle cell disease (SCD), these levels are inversely associated with measures of NO bioavailability. To further evaluate the role of endothelial dysfunction in a population study of SCD, we have measured the levels of soluble endothelium-derived adhesion molecules in the plasma specimens of 160 adult patients with SCD during steady state. Consistent with a link between endothelial dysfunction and end-organ disease, we found that higher levels of soluble vascular cell adhesion molecule-1 (sVCAM-1) were associated with markers indicating renal dysfunction and hepatic impairment. Analysis of soluble intercellular cell adhesion molecule-1 (sICAM-1), sE-selectin and sP-selectin levels indicated partially overlapping associations with sVCAM-1, with an additional association with inflammatory stress and triglyceride levels. Importantly, increased soluble adhesion molecule expression correlated with severity of pulmonary hypertension, a clinical manifestation of endothelial dysfunction. Soluble VCAM-1, ICAM-1, and E-selectin were independently associated with the risk of mortality in this cohort. Our data are consistent with steady state levels of soluble adhesion molecules as markers of pulmonary hypertension and risk of death.

Kato, Gregory J.; Martyr, Sabrina; Blackwelder, William C.; Nichols, James S.; Coles, Wynona A.; Hunter, Lori A.; Brennan, Marie-Luise; Hazen, Stanley L.; Gladwin, Mark T.

2007-01-01

168

Protein kinase A-alpha directly phosphorylates FoxO1 in vascular endothelial cells to regulate expression of vascular cellular adhesion molecule-1 mRNA.  

PubMed

FoxO1, a forkhead box O class transcription factor, is abundant in insulin-responsive tissues. Akt, downstream from phosphatidylinositol 3-kinase in insulin signaling, phosphorylates FoxO1 at Thr(24), Ser(256), and Ser(319), negatively regulating its function. We previously reported that dehydroepiandrosterone-stimulated phosphorylation of FoxO1 in endothelial cells requires cAMP-dependent protein kinase ? (PKA-?). Therefore, we hypothesized that FoxO1 is a novel direct substrate for PKA-?. Using an immune complex kinase assay with [?-(32)P]ATP, purified PKA-? directly phosphorylated wild-type FoxO1 but not FoxO1-AAA (mutant with alanine substitutions at known Akt phosphorylation sites). Phosphorylation of wild-type FoxO1 (but not FoxO1-AAA) was detectable using phospho-specific antibodies. Similar results were obtained using purified GST-FoxO1 protein as the substrate. Thus, FoxO1 is a direct substrate for PKA-? in vitro. In bovine aortic endothelial cells, interaction between endogenous PKA-? and endogenous FoxO1 was detected by co-immunoprecipitation. In human aortic endothelial cells (HAEC), pretreatment with H89 (PKA inhibitor) or siRNA knockdown of PKA-? decreased forskolin- or prostaglandin E(2)-stimulated phosphorylation of FoxO1. In HAEC transfected with a FoxO-promoter luciferase reporter, co-expression of the catalytic domain of PKA-?, catalytically inactive mutant PKA-?, or siRNA against PKA-? caused corresponding increases or decreases in transactivation of the FoxO promoter. Expression of vascular cellular adhesion molecule-1 mRNA, up-regulated by FoxO1 in endothelial cells, was enhanced by siRNA knockdown of PKA-? or treatment of HAEC with the PKA inhibitor H89. Adhesion of monocytes to endothelial cells was enhanced by H89 treatment or overexpression of FoxO1-AAA, similar to effects of TNF-? treatment. We conclude that FoxO1 is a novel physiological substrate for PKA-? in vascular endothelial cells. PMID:21177856

Lee, Ji-Won; Chen, Hui; Pullikotil, Philomena; Quon, Michael J

2011-02-25

169

Endothelial interferon regulatory factor 1 cooperates with NF-kappa B as a transcriptional activator of vascular cell adhesion molecule 1.  

PubMed Central

Transcription of the vascular cell adhesion molecule 1 (VCAM-1) gene in endothelial cells is induced by lipopolysaccharide and the inflammatory cytokines interleukin-1 beta and tumor necrosis factor alpha (TNF-alpha). Previous studies have demonstrated that tandem binding sites for the inducible transcription factor NF-kappa B are necessary but not sufficient for full cytokine-mediated transcriptional activation. Herein, we demonstrate that full cytokine-induced accumulation of VCAM1 transcript requires protein synthesis. We report the definition of a functional regulatory element in the VCAM1 promoter interacting with the transcriptional activator interferon regulatory factor 1 (IRF-1). DNA-protein binding studies with endothelial nuclear extracts revealed that IRF-1 is cytokine inducible and binds specifically to a consensus sequence motif located 3' of the TATA element. We have identified heterodimeric p65 and p50 as the NF-kappa B species binding to the VCAM1 promoter in TNF-alpha-activated endothelial cells. Experiments with recombinant proteins showed that p50/p65 and high-mobility-group I(Y) protein cooperatively facilitated the binding of IRF-1 to the VCAM1 IRF binding site and that IRF-1 physically interacted with p50 and with high-mobility-group I(Y) protein. Transient transfection assay in endothelial cells showed that overexpressed IRF-1 resulted in superinduction of TNF-alpha-stimulated transcription. Site-directed mutations in the IRF binding element decreased TNF-alpha-induced activity and totally abolished superinduction. Cotransfection assays in P19 embryonal carcinoma cells revealed that IRF-1 synergized with p50/p65 NF-kappa B to activate the VCAM1 promoter or heterologous promoter constructs bearing isolated VCAM1 NF-kappa B and IRF binding motifs. Cytokine inducibility of VCAM1 in endothelial cells utilizes the interaction of heterodimeric p50/p65 proteins with IRF-1.

Neish, A S; Read, M A; Thanos, D; Pine, R; Maniatis, T; Collins, T

1995-01-01

170

Intracellular adhesion molecule-1 up-regulation on thyrocytes by iodine of non-obese diabetic.H2(h4) mice is reactive oxygen species-dependent.  

PubMed

Intracellular adhesion molecule-1 (ICAM-1) expression on the thyroid follicular cells of non-obese diabetic (NOD).H2(h4) mice is enhanced by iodide treatment, which correlates with autoimmune thyroid disease in genetically susceptible NOD.H2(h4) mice. The current study examines the mechanism of iodine-enhanced up-regulation of ICAM-1 on the surface of thyroid cells. We hypothesized that the up-regulation of ICAM-1 is due to a transient increase in production of reactive oxygen species (ROS). ROS may initiate signalling of the ICAM-1 gene promoter, enhancing up-regulated ICAM-1 protein on the cell surface. Single-cell suspensions of thyroid follicular cells from thyroiditis-susceptible NOD.H2(h4) or non-susceptible BALB/c mice were treated in vitro with sodium iodide. Extracellular and intracellular ROS were assessed by luminol-derived chemiluminescence and flow cytometry assays respectively. Our results demonstrate that thyroid follicular cells of NOD.H2(h4) generate higher levels of ROS compared with cells from non-susceptible strains of mice. Expression of a subunit protein of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, p67(phox), was analysed by Western blot immunoassay. A constitutive expression of the p67(phox) subunit protein was observed in NOD.H2(h4) mice prior to iodine treatment. No such expression was found in BALB/c mice. Treatment of NOD.H2(h4) thyroid cells with diphenyleneiodium, an inhibitor of NADPH oxidase, reduced generation of ROS and of ICAM-1 protein expression. Thus, thyrocytes from NOD.H2(h4) mice produce enhanced levels of ROS that may be mediated by NADPH oxidase. Consequently, in NOD.H2(h4) mice the ROS-induced signal for ICAM-1 up-regulation may contribute to mononuclear cellular infiltration of the thyroid gland and the progression of autoimmune thyroid disease. PMID:18241232

Sharma, R; Traore, K; Trush, M A; Rose, N R; Burek, C Lynne

2008-04-01

171

Differential regulation of vascular cell adhesion molecule 1 gene expression by specific NF-kappa B subunits in endothelial and epithelial cells.  

PubMed Central

Vascular cell adhesion molecule 1 (VCAM-1) is expressed in both endothelial and epithelial cell types, where it contributes to lymphocyte migration to sites of inflammation. Its expression is regulated by cytokines, in part through two kappa B-like regulatory elements. Because NF-kappa B can be composed of multiple alternative subunits with differential effects on gene expression, the role of different specific NF-kappa B family members subunits in VCAM-1 regulation is unknown. In this report, we define the contribution of different NF-kappa B family members to VCAM-1 gene regulation. We show that both kappa B sites in the VCAM-1 enhancer are required to optimally stimulate gene expression, but the enhancer is differentially regulated by specific combinations of NF-kappa B subunits. At low concentrations, RelA(p65) acted in concert with the approximately 50-kDa product of p105 NF-kappa B, NF-kappa B1(p50), to stimulate transcription, and at high concentrations, RelA(p65) alone stimulated the VCAM-1 promoter. In contrast, NF-kappa B2 inhibited functional activation of the VCAM reporter by p65. Consistent with this finding, an additional binding complex was detected by using recombinant NF-kappa B2(p49)/RelA(p65) with radiolabeled VCAM kappa B site probes. Interestingly, the human immunodeficiency virus enhancer responded differently to stimulation by NF-kappa B subunits, with optimal response to p49(100)/p65. Analysis of NF-kappa B mRNA in human umbilical vein endothelial cells revealed that nfkb1, nfkb2, and relA NF-kappa B but not c-rel were induced by tumor necrosis factor alpha and lipopolysaccharide, which also induce VCAM-1. These data suggest that specific subunits of NF-kappa B regulate VCAM-1 and differentially activate other genes in these cells. Images

Shu, H B; Agranoff, A B; Nabel, E G; Leung, K; Duckett, C S; Neish, A S; Collins, T; Nabel, G J

1993-01-01

172

Detection of vascular cell adhesion molecule-1 expression with USPIO-enhanced molecular MRI in a mouse model of cerebral ischemia.  

PubMed

Vascular damage plays a critical role after stroke, leading notably to edema, hemorrhages and stroke recurrence. Tools to characterize the vascular lesion are thus a real medical need. In this context, the specific nanoparticular contrast agent P03011, an USPIO (ultrasmall superparamagnetic iron oxide) conjugated to a peptide that targets VCAM-1 (vascular cell adhesion molecule-1), was developed to detect this major component of the vascular inflammatory response. This study aimed to make the proof of concept of the capacity of this targeted USPIO to detect VCAM-1 with MRI after cerebral ischemia in mouse. The time course of VCAM-1 expression was first examined by immunohistochemistry in our model of cerebral ischemia-reperfusion. Secondly, P03011 or nontargeted USPIO P03007 were injected 5?h after ischemia (100?µmol iron kg?¹; i.v.) and in vivo and ex vivo MRI were performed 24?h after ischemia onset. Double labeling immunofluorescence was then performed on brain slices in order to detect both USPIO and VCAM-1. VCAM-1 expression was significantly up-regulated 24?h after ischemia in our model. In animals receiving P03011, both in vivo and ex vivo MRI performed 24?h after ischemia onset showed hypointense foci which could correspond to iron particles. Histological analysis showed a co-localization of the targeted USPIO and VCAM-1. This study demonstrates that VCAM-1 detection is possible with the USPIO P03011 in a model of cerebral ischemia. This kind of contrast agent could be an interesting clinical tool to characterize ischemic lesions in terms of vascular damage. PMID:23281288

Fréchou, M; Beray-Berthat, V; Raynaud, J-S; Mériaux, S; Gombert, F; Lancelot, E; Plotkine, M; Marchand-Leroux, C; Ballet, S; Robert, P; Louin, G; Margaill, I

2013-01-01

173

Effect of nuclear factor kappa B on intercellular adhesion molecule-1 expression and neutrophil infiltration in lung injury induced by intestinal ischemia/reperfusion in rats  

PubMed Central

AIM: To investigate the role of nuclear factor kappa B (NF-?B) in the pathogenesis of lung injury induced by intestinal ischemia/reperfusion (I/R), and its effect on intercellular adhesion molecule-1 (ICAM-1) expression and neutrophil infiltration. METHODS: Twenty-four Wistar rats were divided randomly into control, I/R and pyrrolidine dithiocarbamate (PDTC) treatment groups, n?=?8 in each. I/R group and PDTC treatment group received superior mysenteric artery (SMA) occluding for 1 h and reperfusion for 2 h. PDTC group was administrated with intraperitoneal injection of 2% 100 mg/kg PDTC 1 h before surgery. Lung histology and bronchia alveolus lung fluid (BALF) protein were assayed. Serum IL-6, lung malondialdehyde (MDA) and myeloperoxidase (MPO) as well as the expression level of NF-?B and ICAM-1 were measured. RESULTS: Lung injury induced by intestinal I/R, was characterized by edema, hemorrhage and neutrophil infiltration as well as by the significant rising of BALF protein. Compared to control group, the levels of serum IL-6 and lung MDA and MPO increased significantly in I/R group (P?=?0.001). Strong positive expression of NF-?B p65 and ICAM-1 was observed. After the administration of PDTC, the level of serum IL-6, lung MDA and MPO as well as NF-?B and ICAM-1 decreased significantly (P?

Tian, Xiao-Feng; Yao, Ji-Hong; Li, Ying-Hua; Zhang, Xue-Song; Feng, Bing-An; Yang, Chun-Ming; Zheng, Shu-Sen

2006-01-01

174

Heparan sulfates mediate the interaction between platelet endothelial cell adhesion molecule-1 (PECAM-1) and the G?q/11 Subunits of heterotrimeric G proteins.  

PubMed

The endothelial cell-cell junction has emerged as a major cell signaling structure that responds to shear stress by eliciting the activation of signaling pathways. Platelet endothelial cell adhesion molecule-1 (PECAM-1) and heterotrimeric G protein subunits G?q and 11 (G?q/11) are junctional proteins that have been independently proposed as mechanosensors. Our previous findings suggest that they form a mechanosensitive junctional complex that discriminates between different flow profiles. The nature of the PECAM-1·G?q/11 interaction is still unclear although it is likely an indirect association. Here, we investigated the role of heparan sulfates (HS) in mediating this interaction and in regulating downstream signaling in response to flow. Co-immunoprecipitation studies show that PECAM-1·G?q/11 binding is dramatically decreased by competitive inhibition with heparin, pharmacological inhibition with the HS antagonist surfen, and enzymatic removal of HS chains with heparinase III treatment as well as by site-directed mutagenesis of basic residues within the extracellular domain of PECAM-1. Using an in situ proximity ligation assay, we show that endogenous PECAM-1·G?q/11 interactions in endothelial cells are disrupted by both competitive inhibition and HS degradation. Furthermore, we identified the heparan sulfate proteoglycan syndecan-1 in complexes with PECAM-1 that are rapidly decreased in response to flow. Finally, we demonstrate that flow-induced Akt activation is attenuated in endothelial cells in which PECAM-1 was knocked down and reconstituted with a binding mutant. Taken together, our results indicate that the PECAM-1·G?q/11 mechanosensitive complex contains an endogenous heparan sulfate proteoglycan with HS chains that is critical for junctional complex assembly and regulating the flow response. PMID:24497640

dela Paz, Nathaniel G; Melchior, Benot; Shayo, Francisca Y; Frangos, John A

2014-03-14

175

Expression of synaptic cell adhesion molecule 1 (SynCAM 1) in different brain regions in a rat subarachnoid hemorrhage model.  

PubMed

Synapses, the junctions between nerve cells through which they communicate, are formed by the coordinated assembly and tight attachment of pre- and postsynaptic specializations. Synaptic cell adhesion molecule 1 (SynCAM 1) has been proved to be an important factor for synapse function and behavior cognition. The current research aimed to investigate the expression of the SynCAM 1 in the brain after experimental subarachnoid hemorrhage (SAH) in rats. A total of 42 rats were randomly divided into seven groups: control group, sham group, day 1, day 3, day 5, day 7, and day 14 groups. Day 1, day 3, day 5, day 7, and day 14 groups were all SAH groups in which the rats were killed on days 1, 3, 5, 7, and 14, respectively. The rat SAH model was induced by injection of 0.3 ml fresh arterial, non-heparinized blood into the prechiasmatic cistern in 20 s. Immunostaining and immunoblotting experiments were performed to detect the expression of SynCAM 1 protein. The clinical behavior scale was measured on day 14 after SAH. The expression of SynCAM 1 protein was decreased remarkably in SAH groups compared with the sham group. The down-regulated expression of SynCAM 1 was detected after SAH and the low ebb was on days 1-3. The immunohistochemical staining demonstrated expression of SynCAM 1 was present mainly in the neurons in all of the three different regions such as cortex, hippocampus, and cerebellum. The clinical behavior scale was significantly decreased compared with sham rats. Our results indicate that SynCAM 1 expression is down-regulated in the brain after experimental SAH. These finding suggests that decreased SynCAM 1 expression may facilitate the development of cognitive dysfunction after SAH. PMID:23179183

Wang, Zhong; Hu, Tong; Feng, Dongxia; Chen, Gang

2013-08-01

176

Flanking sequences for the human intercellular adhesion molecule-1 NF-kappaB response element are necessary for tumor necrosis factor alpha-induced gene expression.  

PubMed

The regulated expression of intercellular adhesion molecule-1 (ICAM-1) by cytokines such as tumor necrosis factor alpha (TNF-alpha) plays an important role in inflammation and immune responses. Induction of ICAM-1 gene transcription by TNF-alpha has previously been shown to be dependent upon a region of the ICAM-1 5'-flanking sequences that contains a modified kappaB site. We demonstrate here that this modified kappaB site alone is insufficient for induction of transcription by TNF-alpha. Site-directed mutagenesis of both the kappaB site and specific flanking nucleotides demonstrates that both the specific 5'- and 3'-flanking sequences and the modified kappaB site are necessary for TNF-alpha induction. Further, site-directed mutagenesis of this modified kappaB site to a consensus kappaB site allows it to mediate transcriptional activation in response to TNF-alpha, even in the absence of specific flanking sequences. Transcription through this minimal ICAM-1 TNF-alpha-responsive region can be driven by co-expression of p65, and the minimal response element interacts with p65 and p50 in supershift mobility shift assays. However, when in vitro transcription/translation products for the Rel proteins are used in an electrophoretic mobility shift assay, only p65 is capable of binding the minimal response element while both p50 and p65 bind a consensus kappaB oligonucleotide. Additionally, in the absence of the specific flanking nucleotides, the ICAM-1 kappaB site is incapable of DNA-protein complex formation in both electrophoretic mobility shift assay and UV cross-linking/SDS-polyacrylamide gel electrophoresis analysis. These results demonstrate the requirement for specific flanking sequences surrounding a kappaB binding site for functional transcription factor binding and transactivation and TNF-alpha-mediated induction of ICAM-1. PMID:9188493

Paxton, L L; Li, L J; Secor, V; Duff, J L; Naik, S M; Shibagaki, N; Caughman, S W

1997-06-20

177

Gene expression profiles in hypoxic preconditioning using cDNA microarray analysis: altered expression of an angiogenic factor, carcinoembryonic antigen-related cell adhesion molecule 1.  

PubMed

Hypoxic preconditioning has been shown to exhibit cardioprotective effects on myocardium from ischemic or reperfusion injury. The specific regulated gene involved in the hypoxia-induced cardioprotective effects is profiled in this study. Young male Wistar rats and ICR mice were exposed to sea level (as normal control) or simulated high altitude for 15 h/day for 2, 4, or 8 weeks, or for 4 weeks at high altitude after 2 weeks at sea level. The left ventricles of the animals were isolated for mRNA isolation and cDNA microarray analysis. Our data demonstrated that hypoxic preconditioning significantly ameliorated cardiac ischemic injury by minimizing the infarct size. After cluster analysis of expression profiles after different courses of hypoxic preconditioning (0, 2, 4, and 8 weeks), 386 genes showed an ascending pattern, whereas 301 genes showed a descending pattern. The ascending genes include several angiogenic factors: FGF receptor 4, vascular endothelial growth factor (vEGF), and carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM-1). The microvessel density was also significantly increased in hypoxic hearts. Using Western blotting and immunohistochemical analysis, the protein expression level and localization of CEACAM-1 were observed in hypoxic myocardium. The results also indicated that CEACAM-1 was upregulated as with other hypoxic angiogenic factors, heme oxygenase 1 (HO-1) and hypoxia inducible factor-1alpha (HIF-1alpha), in in vitro cultured cardiomyocytes (H9c2) after hypoxia treatment and in vivo hypoxic preconditioning. Furthermore, incubation with recombinant vEGF could also increase the expression level of CEACAM-1 in H9c2 cells. These results demonstrated that hypoxic preconditioning resulted in transcriptional changes, and some of these genes have been correlated with angiogenesis. The HIF-1/vEGF/CEACAM-1 pathway might be important for hypoxia-induced angiogenesis in the heart during hypoxic preconditioning. PMID:16044082

Chen, Wen-Jone; Chen, Huei-Wen; Yu, Sung-Liang; Huang, Chien-Hua; Wang, Tzung-Dau; Chen, Jeremy J W; Chien, Chiang-Ting; Chen, Hsuan-Yu; Yang, Pan-Chyr; Lee, Yuan-Teh

2005-08-01

178

Increased Ectodomain Shedding of Cell Adhesion Molecule 1 from Pancreatic Islets in Type 2 Diabetic Pancreata: Correlation with Hemoglobin A1c Levels  

PubMed Central

Pulmonary emphysema and type 2 diabetes mellitus (T2DM), both caused by lifestyle factors, frequently concur. Respectively, the diseases affect lung alveolar and pancreatic islet cells, which express cell adhesion molecule 1 (CADM1), an immunoglobulin superfamily member. Protease-mediated ectodomain shedding of full-length CADM1 produces C-terminal fragments (CTFs) with proapoptotic activity. In emphysematous lungs, the CADM1 shedding rate and thus the level of CTFs in alveolar cells increase. In this study, CADM1 expression in islet cells was examined by western blotting. Protein was extracted from formalin-fixed, paraffin-embedded sections of pancreata isolated from patients with T2DM (n?=?12) or from patients without pancreatic disease (n?=?8) at autopsy. After adjusting for the number of islet cells present in the adjacent section, we found that full-length CADM1 decreased in T2DM islets, while ectodomain shedding increased. Hemoglobin A1c levels, measured when patients were alive, correlated inversely with full-length CADM1 levels (P?=?0.041) and positively with ectodomain shedding rates (P?=?0.001). In immunofluorescence images of T2DM islet cells, CADM1 was detected in the cytoplasm, but not on the cell membrane. Consistently, when MIN6-m9 mouse beta cells were treated with phorbol ester and trypsin to induce shedding, CADM1 immunostaining was diffuse in the cytoplasm. When a form of CTFs was exogenously expressed in MIN6-m9 cells, it localized diffusely in the cytoplasm and increased the number of apoptotic cells. These results suggest that increased CADM1 ectodomain shedding contributes to blood glucose dysregulation in T2DM by decreasing full-length CADM1 and producing CTFs that accumulate in the cytoplasm and promote apoptosis of beta cells. Thus, this study has identified a molecular alteration shared by pulmonary emphysema and T2DM.

Yoneshige, Azusa; Kato, Takashi; Enoki, Eisuke; Maenishi, Osamu; Chikugo, Takaaki; Kimura, Masatomo; Satou, Takao; Ito, Akihiko

2014-01-01

179

Intercellular adhesion molecule-1 on synovial cells attenuated interleukin-6-induced inhibition of osteoclastogenesis induced by receptor activator for nuclear factor ?B ligand  

PubMed Central

In a co-culture of osteoclast precursor cells and synovial cells, interleukin-6 (IL-6) induces osteoclast formation. In contrast, in a monoculture of osteoclast precursor cells, IL-6 directly suppresses receptor activator for nuclear factor ?B ligand (RANKL)-induced differentiation of osteoclast precursor cells into osteoclasts. In the present study, we explored why the effect of IL-6 differed between the monoculture and the co-culture systems. In the monoculture, mouse osteoclast precursor cell line, RAW 264·7 (RAW) cells were cultured with soluble RANKL (sRANKL) for 24 h or 3 days. sRANKL increased both expression of osteoclastogenesis marker, tartrate-resistant acid phosphatase isoform 5b (TRAP5b) and nuclear factor of activated T cells cytoplasmic 1 (NFATc1), whereas the co-addition of IL-6 decreased them both in a dose-dependent manner. In the co-culture, RAW cells and human synovial cell line, SW982 cells were cultured with IL-6 + soluble IL-6 receptor (sIL-6R) for 3 days. TRAP5b and NFATc1 expression reduced by IL-6 was increased by the addition of SW982 cells in a manner dependent upon the number of added cells. IL-6 + sIL-6R treatment significantly induced RANKL production in SW982 cells, and anti-RANKL antibody inhibited IL-6 + sIL-6R-induced osteoclastogenesis. SW982 cells expressed high levels of ICAM-1 originally, and ICAM-1 expression was increased significantly by IL-6 + sIL-6R. Anti-ICAM-1 antibody suppressed IL-6-induced osteoclastogenesis. Finally, in the monoculture system, addition of sICAM-1 dose-dependently restored the expression of TRAP5b reduced by IL-6. Similar results were obtained when the formation of TRAP-positive multi-nuclear cells were examined using mouse bone marrow cells. In conclusion, IL-6 gave different results in the co-culture and monoculture systems because in the co-culture, ICAM-1 from the synovial cells restored osteoclastogenesis suppressed by IL-6.

Suzuki, M; Hashizume, M; Yoshida, H; Shiina, M; Mihara, M

2011-01-01

180

Intercellular adhesion molecule-1 on synovial cells attenuated interleukin-6-induced inhibition of osteoclastogenesis induced by receptor activator for nuclear factor ?B ligand.  

PubMed

In a co-culture of osteoclast precursor cells and synovial cells, interleukin-6 (IL-6) induces osteoclast formation. In contrast, in a monoculture of osteoclast precursor cells, IL-6 directly suppresses receptor activator for nuclear factor ?B ligand (RANKL)-induced differentiation of osteoclast precursor cells into osteoclasts. In the present study, we explored why the effect of IL-6 differed between the monoculture and the co-culture systems. In the monoculture, mouse osteoclast precursor cell line, RAW 264·7 (RAW) cells were cultured with soluble RANKL (sRANKL) for 24 h or 3 days. sRANKL increased both expression of osteoclastogenesis marker, tartrate-resistant acid phosphatase isoform 5b (TRAP5b) and nuclear factor of activated T cells cytoplasmic 1 (NFATc1), whereas the co-addition of IL-6 decreased them both in a dose-dependent manner. In the co-culture, RAW cells and human synovial cell line, SW982 cells were cultured with IL-6+soluble IL-6 receptor (sIL-6R) for 3 days. TRAP5b and NFATc1 expression reduced by IL-6 was increased by the addition of SW982 cells in a manner dependent upon the number of added cells. IL-6+sIL-6R treatment significantly induced RANKL production in SW982 cells, and anti-RANKL antibody inhibited IL-6+sIL-6R-induced osteoclastogenesis. SW982 cells expressed high levels of ICAM-1 originally, and ICAM-1 expression was increased significantly by IL-6+sIL-6R. Anti-ICAM-1 antibody suppressed IL-6-induced osteoclastogenesis. Finally, in the monoculture system, addition of sICAM-1 dose-dependently restored the expression of TRAP5b reduced by IL-6. Similar results were obtained when the formation of TRAP-positive multi-nuclear cells were examined using mouse bone marrow cells. In conclusion, IL-6 gave different results in the co-culture and monoculture systems because in the co-culture, ICAM-1 from the synovial cells restored osteoclastogenesis suppressed by IL-6. PMID:21039424

Suzuki, M; Hashizume, M; Yoshida, H; Shiina, M; Mihara, M

2011-01-01

181

Function and evolutionary conservation of distinct epitopes on the leukocyte adhesion molecule-1 (TQ-1, Leu-8) that regulate leukocyte migration.  

PubMed

The leukocyte adhesion molecule-1 (LAM-1, TQ=1, Leu-8) in humans, like its murine homologue, MEL-14, is the principal receptor that mediates the binding of leukocytes to high endothelial venules (HEV) of peripheral lymph nodes. In this study, several regions of the protein which mediate receptor function were identified by using a large panel of murine mAb reactive with LAM-1. Individual mAb reacted with LAM-1+ cells with characteristic intensities of immunofluorescence staining, and each bound both lymphocytes and neutrophils. Lymphocyte attachment to HEV was significantly inhibited by the binding of five mAb. In contrast, only two of these mAb were able to completely block the binding of phosphomannan monoester core complex from the yeast Hansenula holstii cell wall (PPME), a phosphomannan monoester core polysaccharide that serves as a soluble model of the natural ligand of LAM-1. Interestingly, the binding of two anti-LAM-1 mAb to cells induced a significant increase in PPME binding, reminiscent of the increase in receptor affinity observed after leukocyte activation. Antibody cross-blocking studies indicated that many of the functionally important epitopes were spatially distinct, and domain mapping indicated that they recognized distinct domains of LAM-1. The expression and function of these epitopes were further assessed by using a variety of animal species to further characterize the functionally relevant epitopes defined in these studies. At least some anti-LAM-1 mAb reacted with leukocytes from monkey, cow, rabbit, sheep, dog, cat, pig, and goat, but not from chicken, rat, or mouse. The reactivity of anti-LAM-1 mAb in several animal species correlated with the ability of leukocytes to bind PPME, and mAb that inhibited lymphocyte binding to HEV in man could also inhibit this function in rhesus monkey and dog. Thus, several LAM-1 epitopes are structurally and functionally well conserved throughout recent mammalian evolution, emphasizing an important role for LAM-1 in the regulation of leukocyte traffic. PMID:1713609

Spertini, O; Kansas, G S; Reimann, K A; Mackay, C R; Tedder, T F

1991-08-01

182

A Phase II Trial of Fosbretabulin in Advanced Anaplastic Thyroid Carcinoma and Correlation of Baseline Serum-Soluble Intracellular Adhesion Molecule-1 with Outcome  

PubMed Central

Background Fosbretabulin is a novel vascular-disrupting agent that has antitumor activity against anaplastic thyroid cancer (ATC) cell lines, xenografts, and demonstrable efficacy in a phase I trial. This phase II study determined the efficacy and safety of fosbretabulin in patients with advanced ATC and whether fosbretabulin altered the natural history of ATC by virtue of doubling the median survival. A secondary aim evaluated the prognostic value of serum soluble intracellular adhesion molecule-1 (sICAM). Methods Twenty-six patients received fosbretabulin 45?mg/m2 as a 10-minute intravenous infusion on days 1, 8, and 15 of a 28-day cycle. sICAM levels were obtained at baseline, over the first two cycles, and end of therapy. Treatment was continued until disease progression. Results Fosbretabulin was well tolerated; grade 3 toxicity was observed in nine patients (35%), and grade 4 toxicity in one (4%). QTc prolongation delayed treatment in four causing one to stop treatment. Median survival was 4.7 months with 34% and 23% alive at 6 and 12 months, respectively. Median duration of stable disease in seven patients was 12.3 months (range, 4.4–37.9 months). Baseline serum sICAM levels were measured in 24 patients with a median 253.5?ng/mL. There was a significant difference in event-free survival among tertiles of baseline sICAM levels (p?

Mooney, Colin J.; Nagaiah, Govardhanan; Fu, Pingfu; Wasman, Jay K.; Cooney, Matthew M.; Savvides, Panos S.; Bokar, Joseph A.; Dowlati, Afshin; Wang, Ding; Agarwala, Sanjiv S.; Flick, Susan M.; Hartman, Paul H.; Ortiz, Jose D.; Lavertu, Pierre N.

2009-01-01

183

Ultraviolet radiation can either suppress or induce expression of intercellular adhesion molecule 1 (ICAM-1) on the surface of cultured human keratinocytes  

SciTech Connect

Interactions of the ligand/receptor pair LFA-1(CD11a/CD18) and ICAM-1(CD54) initiate and control the cell-cell interactions of leukocytes and interactions of leukocytes with parenchymal cells in all phases of the immune response. Induction of the intercellular adhesion molecule 1 (ICAM-1) on the surface of epidermal keratinocytes has been proposed as an important regulator of contact-dependent aspects of cutaneous inflammation. Ultraviolet radiation (UVR) also modifies cutaneous inflammation, producing both up- and down-regulation of contact hypersensitivity. We have found that UVR has a biphasic effect on the induction of keratinocyte CD54. Using immunofluorescence and FACS techniques to quantitate cell-surface CD54 staining, we have shown that UVR significantly (p less than 0.01) inhibits keratinocyte CD54 induction by gamma interferon 24 h after irradiation. However, at 48, 72, and 96 h after UVR, CD54 expression is significantly induced to levels even greater than are induced by gamma interferon (20 U/ml). In addition, at 48, 72, or 96 h following UVR (30-100 mJ/cm2), the gamma-interferon-induced CD54 expression on human keratinocytes is also strongly (p less than 0.05 to p less than 0.001) enhanced. In this cell-culture system, gamma interferon and TNF-alpha are both strong CD54 inducers and are synergistic, but GM-CSF, TFG-beta, and IL-1 have no direct CD54-inducing effects. Thus the effects of UVR on CD54 induction are biphasic, producing inhibition at 24 h and induction at 48, 72, and 96 h. This effect on CD54 may contribute to the biphasic effects of UVR on delayed hypersensitivity in vivo. The early inhibition of ICAM-1 by UVR may also contribute to the therapeutic effects of UVR. We also speculate that the late induction of ICAM-1 by UVR might be an important step in the induction of photosensitive diseases such as lupus erythematosus.

Norris, D.A.; Lyons, M.B.; Middleton, M.H.; Yohn, J.J.; Kashihara-Sawami, M. (Univ. of Colorado Health Sciences Center, Denver (USA))

1990-08-01

184

Plasma asymmetric dimethylarginine (ADMA) concentration is independently associated with carotid intima-media thickness and plasma soluble vascular cell adhesion molecule-1 (sVCAM-1) concentration in patients with mild-to-moderate renal failure  

Microsoft Academic Search

Plasma asymmetric dimethylarginine (ADMA) concentration is independently associated with carotid intima-media thickness and plasma soluble vascular cell adhesion molecule-1 (sVCAM-1) concentration in patients with mild-to-moderate renal failure.BackgroundPatients with renal insufficiency have an increased risk of cardiovascular disease that is not fully explained by the presence of known cardiovascular risk factors. In patients with end-stage renal disease, increased serum concentration of

PRABATH W B NANAYAKKARA; TOM TEERLINK; COEN D A STEHOUWER; DAUD ALLAJAR; ANNEMIEKE SPIJKERMAN; CASPER SCHALKWIJK; PIET M TER WEE; COEN VAN GULDENER

2005-01-01

185

Soluble Intercellular Adhesion Molecules, Soluble Vascular Cell Adhesion Molecules, and Risk of Coronary Heart Disease  

Microsoft Academic Search

Objective: We examined the association of circulating levels of soluble intercellular adhesion molecules (sICAM-1) and soluble vascular cell adhesion molecules (sVCAM-1) with coronary heart disease (CHD) risk factors and whether the adhesion molecules alone, and in combination, can serve as predictors of coronary CHD.Research Methods and Procedures: Among 18,225 men from the Health Professional Follow-up Study who provided blood in

Iris Shai; Tobias Pischon; Frank B. Hu; Alberto Ascherio; Nader Rifai; Eric B. Rimm

2006-01-01

186

The second domain of intercellular adhesion molecule-1 (ICAM-1) maintains the structural integrity of the leucocyte function-associated antigen-1 (LFA-1) ligand-binding site in the first domain.  

PubMed Central

The first domain of intercellular adhesion molecule-1 (ICAM-1) binds to the leucocyte function-associated antigen-1 (LFA-1) I domain, which contains the principal ligand-binding site of this leucocyte integrin. Whether the function of the second domain is also to directly bind LFA-1 has been unclear. Our data show that mutation in the hydrophilic EF loop of ICAM-1 domain 2 resulted in impaired binding of the isolated I domain when compared with wild-type ICAM-1. LFA-1 on T-cells also binds with reduced affinity to this ICAM-1 mutant. A hybrid construct containing the first domain of vascular cell-adhesion molecule-1 joined to domains 2-5 of ICAM-1 was unable to bind to the I domain, showing that there is no direct interaction between the second domain of ICAM-1 and the I domain. This construct was also not bound by LFA-1 expressed in T-cells. Function-blocking monoclonal antibodies that map to domain 2 of ICAM-1, implicating this domain in ligand binding, were found to act indirectly. In summary our data suggest that the second domain of ICAM-1 has a role in maintaining the structure of the LFA-1 ligand-binding site in the first domain of ICAM-1 but does not appear to have a direct role in ligand binding.

Stanley, P; McDowall, A; Bates, P A; Brashaw, J; Hogg, N

2000-01-01

187

Arrangement of Domains, and Amino Acid Residues Required for Binding of Vascular Cell Adhesion Molecule1 to Its Counter-Receptor VLA4 (a4fll)  

Microsoft Academic Search

Interaction of the vascular cell adhesion molecule (VCAM-1) with its counter-receptor very late antigen-4 (VLA-4) (integrin ot4fl0 is important for a number of developmental pathways and inflammatory functions. We are investigating the molecular mecha- nism of this binding, in the interest of developing new anti-inflammatory drugs that block it. In a previous report, we showed that the predominant form of

Laurelee Osborn; Cornelia Vassallo; Beth Grifliths Browning; Richard Tizard; Dorian O. Haskard; Christopher D. Benjamin; Irene Dougas; Tomas Kirchhausen

1994-01-01

188

Inhibition of antigen-receptor signaling by Platelet Endothelial Cell Adhesion Molecule1 (CD31) requires functional ITIMs, SHP2, and p56lck  

Microsoft Academic Search

Platelet Endothelial Cell Adhesion Mole- cule-1 (PECAM-1, CD31) is a 130-kd member of the immunoglobulin gene superfamily that is expressed on the surface of platelets, endothelial cells, myeloid cells, and certain lymphocyte subsets. PECAM-1 has recently been shown to contain functional immuno- receptor tyrosine-based inhibitory motifs (ITIMs) within its cytoplasmic domain, and co-ligation of PECAM-1 with the T-cell anti- gen

Debra K. Newman; Christin Hamilton; Peter J. Newman

189

Pentosan polysulfate treatment ameliorates motor function with increased serum soluble vascular cell adhesion molecule-1 in HTLV-1-associated neurologic disease.  

PubMed

The main therapeutic strategy against human T lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) characterized by lower extremity motor dysfunction is immunomodulatory treatment, with drugs such as corticosteroid hormone and interferon-?, at present. However, there are many issues in long-term treatment with these drugs, such as insufficient effects and various side effects. We now urgently need to develop other therapeutic strategies. The heparinoid, pentosan polysulfate sodium (PPS), has been safely used in Europe for the past 50 years as a thrombosis prophylaxis and for the treatment of phlebitis. We conducted a clinical trial to test the effect of subcutaneous administration of PPS in 12 patients with HAM/TSP in an open-labeled design. There was a marked improvement in lower extremity motor function, based on reduced spasticity, such as a reduced time required for walking 10 m and descending a flight of stairs. There were no significant changes in HTLV-I proviral copy numbers in peripheral blood contrary to the inhibitory effect of PPS in vitro for intercellular spread of HTLV-I. However, serum soluble vascular cell adhesion molecule (sVCAM)-1 was significantly increased without significant changes of serum level of chemokines (CXCL10 and CCL2). There was a positive correlation between increased sVCAM-1and reduced time required for walking 10 m. PPS might induce neurological improvement by inhibition of chronic inflammation in the spinal cord, through blocking the adhesion cascade by increasing serum sVCAM-1, in addition to rheological improvement of the microcirculation. PPS has the potential to be a new therapeutic tool for HAM/TSP. PMID:24671717

Nakamura, Tatsufumi; Satoh, Katsuya; Fukuda, Taku; Kinoshita, Ikuo; Nishiura, Yoshihiro; Nagasato, Kunihiko; Yamauchi, Atsushi; Kataoka, Yasufumi; Nakamura, Tadahiro; Sasaki, Hitoshi; Kumagai, Kenji; Niwa, Masami; Noguchi, Mitsuru; Nakamura, Hideki; Nishida, Noriyuki; Kawakami, Atsushi

2014-06-01

190

Triamcinolone acetonide modulates permeability and intercellular adhesion molecule-1 (ICAM-1) expression of the ECV304 cell line: implications for macular degeneration  

PubMed Central

Whilst animal studies and a pilot clinical trial suggest that intravitreal triamcinolone acetonide (TA) may be useful in the treatment of age-related macular degeneration (AMD), its mode of action remains to be fully elucidated. The present study has investigated the capacity of TA to modulate the expression of adhesion molecules and permeability using a human epithelial cell line (ECV304) as a model of the outer blood–retinal barrier (BRB). The influence of TA on the expression of ICAM-1 and MHC-I was studied on resting and phorbol myristate acetate (PMA)- or interferon-gamma (IFN-?)- and/or tumour necrosis factor-alpha (TNF-?)-activated cells using flow cytometry and immunocytochemistry. Additionally, ECV304 cells were grown to confluence in uncoated Transwell chambers; transepithelial resistance (TER) across resting and PMA-activated cells was monitored. TA significantly decreased the paracellular permeability of ECV304 cells and down-regulated ICAM-1 expression, consistent with immunocytochemical observations. PMA-induced permeability changes were dose-dependent and TA decreased permeability of both resting and PMA-activated monolayers. MHC-I expression by ECV304 cells however, was not significantly affected by TA treatment. The modulation of TER and ICAM-1 expression in vitro correlate with clinical observations, suggesting re-establishment of the BRB and down-regulation of inflammatory markers are the principal effects of intravitreal TA in vivo. The results further indicate that TA has the potential to influence cellular permeability, including the barrier function of the retinal pigment epithelium (RPE) in AMD-affected retinae.

Penfold, P L; Wen, L; Madigan, M C; Gillies, M C; King, N J. C; Provis, J M

2000-01-01

191

Arrangement of domains, and amino acid residues required for binding of vascular cell adhesion molecule-1 to its counter-receptor VLA-4 (alpha 4 beta 1)  

PubMed Central

Interaction of the vascular cell adhesion molecule (VCAM-1) with its counter-receptor very late antigen-4 (VLA-4) (integrin alpha 4 beta 1) is important for a number of developmental pathways and inflammatory functions. We are investigating the molecular mechanism of this binding, in the interest of developing new anti-inflammatory drugs that block it. In a previous report, we showed that the predominant form of VCAM-1 on stimulated endothelial cells, seven-domain VCAM (VCAM-7D), is a functionally bivalent molecule. One binding site requires the first and the other requires the homologous immunoglobulin-like domain. Rotary shadowing and electron microscopy of recombinant soluble VCAM-7D molecules suggests that the seven Ig-like domains are extended in a slightly bent linear array, rather than compactly folded together. We have systematically mutagenized the first domain of VCAM-6D (a monovalent, alternately spliced version mission domain 4) by replacing 3-4 amino acids of the VCAM sequence with corresponding portions of the related ICAM-1 molecule. Specific amino acids, important for binding VLA-4 include aspartate 40 (D40), which corresponds to the acidic ICAM- 1 residue glutamate 34 (E34) previously reported to be essential for binding of ICAM-1 to its integrin counter-receptor LFA-1. A small region of VCAM including D40, QIDS, can be replaced by the similar ICAM- 1 sequence, GIET, without affecting function or epitopes, indicating that this region is part of a general integrin-binding structure rather than a determinant of binding specificity for a particular integrin. The VCAM-1 sequence G65NEH also appears to be involved in binding VLA-4.

1994-01-01

192

Cholestin (Monascus purpureus rice) inhibits homocysteine-induced reactive oxygen species generation, nuclear factor-kappaB activation, and vascular cell adhesion molecule-1 expression in human aortic endothelial cells.  

PubMed

Hyperhomocysteinemia is associated with dysfunction and an independent risk factor of cardiovascular diseases. Cholestin (Monascus purpureus-fermented rice), contains a naturally-occurring statin, which has lipid-modulating and anti-inflammatory effects. We investigated the effects of Cholestin extract on the expression of vascular cell adhesion molecule-1 (VCAM-1) by homocysteine (HCY)-treated human aortic endothelial cells (HAECs). Supplement of HAECs with Cholestin extract significantly suppressed cellular binding between the human monocytic cells U937 and HCY-stimulated HAECs. Quantitative PCR and immunoblot analysis showed that Cholestin extract significantly attenuated HCY-induced expression of VCAM-1 mRNA and protein, respectively. Gel shift assays showed that Cholestin treatment reduced HCY-activated transcription factor nuclear factor-kappaB (NF-kappaB). Furthermore, Cholestin also attenuated reactive oxygen species (ROS) generation in vitro and in HCY-treated HAECs. Supplement with statins including simvastatin and parastatin gave similar results as compared with Cholestin. In conclusion, Cholestin reduces HCY-stimulated endothelial adhesiveness as well as downregulating intracellular ROS formation, NF-kappaB activation, and VCAM-1 expression in HAECs, supporting the notion that the natural compound Cholestin may have potential implications in clinical atherosclerosis disease. PMID:17906965

Lin, Chih-Pei; Chen, Yung-Hsiang; Chen, Jaw-Wen; Leu, Hsin-Bang; Liu, Tsan-Zon; Liu, Po-Len; Huang, Song-Lih

2008-03-01

193

Ursolic acid, a natural pentacyclic triterpenoid, inhibits intracellular trafficking of proteins and induces accumulation of intercellular adhesion molecule-1 linked to high-mannose-type glycans in the endoplasmic reticulum.  

PubMed

Ursolic acid (3?-hydroxy-urs-12-en-28-oic acid) is a natural pentacyclic triterpenoid that is present in many plants, including medicinal herbs, and foods. Ursolic acid was initially identified as an inhibitor of the expression of intercellular adhesion molecule-1 (ICAM-1) in response to interleukin-1? (IL-1?). We report here a novel biological activity: ursolic acid inhibits intracellular trafficking of proteins. Ursolic acid markedly inhibited the IL-1?-induced cell-surface ICAM-1 expression in human cancer cell lines and human umbilical vein endothelial cells. By contrast, ursolic acid exerted weak inhibitory effects on the IL-1?-induced ICAM-1 expression at the protein level. Surprisingly, we found that ursolic acid decreased the apparent molecular weight of ICAM-1 and altered the structures of N-linked oligosaccharides bound to ICAM-1. Ursolic acid induced the accumulation of ICAM-1 in the endoplasmic reticulum, which was linked mainly to high-mannose-type glycans. Moreover, in ursolic-acid-treated cells, the Golgi apparatus was fragmented into pieces and distributed over the cells. Thus, our results reveal that ursolic acid inhibits intracellular trafficking of proteins and induces the accumulation of ICAM-1 linked to high-mannose-type glycans in the endoplasmic reticulum. PMID:24649404

Mitsuda, Satoshi; Yokomichi, Tomonobu; Yokoigawa, Junpei; Kataoka, Takao

2014-01-01

194

CD38/CD31, the CCL3 and CCL4 chemokines, and CD49d/vascular cell adhesion molecule-1 are interchained by sequential events sustaining chronic lymphocytic leukemia cell survival.  

PubMed

CD38 and CD49d are associated negative prognosticators in chronic lymphocytic leukemia (CLL). Despite evidence that both molecules are involved in interactions occurring between CLL and normal cells in the context of CLL-involved tissues, a functional link is still missing. Using gene expression profiles comparing CD38(+)CD49d(+) versus CD38(-)CD49d(-) CLL cells, we showed overexpression of the CCL3 and CCL4 chemokines in cells from the former group. These chemokines were also up-regulated by CD38 signals in CLL; moreover, CCL3 was expressed by CLL cells from bone marrow biopsies (BMB) of CD38(+)CD49d(+) but not CD38(-)CD49d(-) cases. High levels of CCR1 and, to a lesser extent, CCR5, the receptors for CCL3 and CCL4, were found in CLL-derived monocyte-macrophages. Consistently, CCL3 increased monocyte migration, and CD68(+) macrophage infiltration was particularly high in BMB from CD38(+)CD49d(+) CLL. Conditioned media from CCL3-stimulated macrophages induced endothelial cells to express vascular cell adhesion molecule-1 (VCAM-1), the CD49d ligand, likely through tumor necrosis factor alpha overproduction. These effects were apparent in BMB from CD38(+)CD49d(+) CLL, where lymphoid infiltrates were characterized by a prominent meshwork of VCAM-1(+) stromal/endothelial cells. Lastly, CD49d engagement by VCAM-1 transfectants increased viability of CD38(+)CD49d(+) CLL cells. Altogether, CD38 and CD49d can be thought of as parts of a consecutive chain of events ultimately leading to improved survival of CLL cells. PMID:19383907

Zucchetto, Antonella; Benedetti, Dania; Tripodo, Claudio; Bomben, Riccardo; Dal Bo, Michele; Marconi, Daniela; Bossi, Fleur; Lorenzon, Debora; Degan, Massimo; Rossi, Francesca Maria; Rossi, Davide; Bulian, Pietro; Franco, Vito; Del Poeta, Giovanni; Deaglio, Silvia; Gaidano, Gianluca; Tedesco, Francesco; Malavasi, Fabio; Gattei, Valter

2009-05-01

195

Zinc oxide nanoparticles-induced intercellular adhesion molecule 1 expression requires Rac1/Cdc42, mixed lineage kinase 3, and c-Jun N-terminal kinase activation in endothelial cells.  

PubMed

The explosive development of nanotechnology has caused an increase in unintended biohazards in humans and in the ecosystem. Similar to particulate matter, nanoparticles (NPs) are strongly correlated with the increase in incidences of cardiovascular diseases, yet the mechanisms behind this correlation remain unclear. Within the testing concentrations of 0.1-10 ?g/ml, which did not cause a marked drop in cell viability, zinc oxide NPs (ZnO-NPs) induced intercellular adhesion molecule-1 (ICAM-1) messenger RNA, and protein expression in both concentration- and time-dependent manner in treated human umbilical vein endothelial cells (HUVECs). ZnO-NPs treatment cause the activation of Ras-related C3 botulinum toxin substrate 1 (Rac1)/cell division control protein 42 homolog (Cdc42) and protein accumulation of mixed lineage kinase 3 (MLK3), followed by c-Jun N-terminal kinase (JNK) and transcription factor c-Jun activation. Induction of ICAM-1 and phosphorylation of JNK and c-Jun could be inhibited by either JNK inhibitor SP600125 or Rac guanosine triphosphatase inhibitor NSC23766 pretreatment. In addition, pretreatment with NSC23766 significantly reduced MLK3 accumulation, suggesting the involvement of Rac1/Cdc42-MLK3-JNK-c-Jun signaling in the regulation of ZnO-NPs-induced ICAM-1 expression, whereas these signaling factors were not activated in zinc oxide microparticles (ZnO-MPs)-treated HUVECs. The increase of ICAM-1 expression on ZnO-NPs-treated HUVECs enables leukocytes to adhere and has been identified as an indicator of vascular inflammation. Our data are essential for safety evaluation of the clinical usage of ZnO-NPs in daily supplements, cosmetics, and biomedicines. PMID:22166487

Li, Ching-Hao; Liao, Po-Lin; Shyu, Ming-Kwang; Liu, Chen-Wei; Kao, Chen-Chieh; Huang, Shih-Hsuan; Cheng, Yu-Wen; Kang, Jaw-Jou

2012-03-01

196

Mechanistic Control of Carcinoembryonic Antigen-related Cell Adhesion Molecule-1 (CEACAM1) Splice Isoforms by the Heterogeneous Nuclear Ribonuclear Proteins hnRNP L, hnRNP A1, and hnRNP M*  

PubMed Central

Carcinoembryonic antigen-related cell adhesion molecule-1 (CEACAM1) is expressed in a variety of cell types and is implicated in carcinogenesis. Alternative splicing of CEACAM1 pre-mRNA generates two cytoplasmic domain splice variants characterized by the inclusion (L-isoform) or exclusion (S-isoform) of exon 7. Here we show that the alternative splicing of CEACAM1 pre-mRNA is regulated by novel cis elements residing in exon 7. We report the presence of three exon regulatory elements that lead to the inclusion or exclusion of exon 7 CEACAM1 mRNA in ZR75 breast cancer cells. Heterologous splicing reporter assays demonstrated that the maintenance of authentic alternative splicing mechanisms were independent of the CEACAM1 intron sequence context. We show that forced expression of these exon regulatory elements could alter CEACAM1 splicing in HEK-293 cells. Using RNA affinity chromatography, three members of the heterogeneous nuclear ribonucleoprotein family (hnRNP L, hnRNP A1, and hnRNP M) were identified. RNA immunoprecipitation of hnRNP L and hnRNP A1 revealed a binding motif located central and 3? to exon 7, respectively. Depletion of hnRNP A1 or L by RNAi in HEK-293 cells promoted exon 7 inclusion, whereas overexpression led to exclusion of the variable exon. By contrast, overexpression of hnRNP M showed exon 7 inclusion and production of CEACAM1-L mRNA. Finally, stress-induced cytoplasmic accumulation of hnRNP A1 in MDA-MB-468 cells dynamically alters the CEACAM1-S:CEACAM1:L ratio in favor of the l-isoform. Thus, we have elucidated the molecular factors that control the mechanism of splice-site recognition in the alternative splicing regulation of CEACAM1.

Dery, Kenneth J.; Gaur, Shikha; Gencheva, Marieta; Yen, Yun; Shively, John E.; Gaur, Rajesh K.

2011-01-01

197

Pentoxifylline-induced modulation of melanoma cell growth, adhesion and lymphokine activated killer cell-mediated lysis.  

PubMed

Pentoxifylline (PX) is a phosphodiesterase inhibitor which effectively increases overall cAMP levels within the cell. This study analyses the ability of PX to alter growth, adhesion and lymphokine activated killer (LAK) cell-mediated lysis of the C8161 and Hs294T human melanoma cell lines, and investigates the role of intercellular adhesion molecule-1 (ICAM-1) in the tumour/LAK cell interaction. We have demonstrated that 4 days' pretreatment with PX (100-250 microg/ml) significantly reduces cell numbers in a dose- and time-dependent manner, with cell numbers decreasing by 67.5% in the C8161 cell line and by 65.4% in the Hs294T cell line with 250 microg/ml PX. Adherence of both cell lines to a range of extracellular matrix components is not affected by PX, with the exception of the C8161 cells, where 4 days' pretreatment with 250 microg/ml PX causes a 24.2% reduction in adherence to fibronectin. Four days' pretreatment of the tumour cells with 250 microg/ml PX leads to increased lysis of the C8161 cells and decreased lysis of the Hs294T cells. The addition of blocking ICAM-1 antibody (10 microg/ml) to the C8161 cells at an effector:tumour cell ratio of 40:1 causes a 2.3-fold reduction in lysis of both control and PX-treated cells. Addition of blocking ICAM-1 antibody (5 microg/ml) to Hs294T cells reduces lysis of control cells 1.8-fold. In PX-treated Hs294T cells, 10 microg/ml of blocking ICAM-1 antibody significantly reduces lysis 1.5-fold. The more aggressive C8161 cells produce 5-fold greater levels of soluble ICAM-1 (sICAM-1) than the poorly metastatic Hs294T cells. PX (10-250 microg/ml) causes a dose-dependent increase in sICAM-1 expression in both cell lines, with maximum increases of 4.7-fold and 4.3-fold in the Hs294T and C8161 cell lines, respectively, following 4 days' pretreatment with 250 microg/ml PX. Collectively, these data demonstrate the ability of PX to alter tumour cell growth, adhesion and LAK cell-mediated lysis and also support a role for the involvement of ICAM-1 in the tumour/LAK cell interaction. PMID:10338332

Alexander, C L; Edward, M; MacKie, R M

1999-02-01

198

Serum levels of adhesion molecules in children and adolescents with immune and non-immune thyroid diseases.  

PubMed

Serum levels of sICAM-1, sVCAM-1 and sP-selectin were determined in patients with Graves' disease before and after 8 weeks and 24 months of methimazole therapy, in levothyroxine suppressed patients with non-toxic nodular goiter, and in a group of healthy controls, to elucidate the relationship to circulating antithyroid antibodies and possible role of soluble adhesion molecules as markers of inflammatory activity. sICAM-1, sVCAM-1, and sP-selectin in patients with untreated hyperthyroidism were markedly elevated compared with controls. After 8 weeks of methimazole treatment, the concentrations of these molecules dropped, but were still significantly higher than in healthy children. In patients with clinical and biochemical remission after 24 months of therapy, sICAM-1 values were on the verge of significance, but still higher than in the control group, whereas serum levels of sVCAM-1 and sP-selectin had normalized. Slightly higher serum sICAM-1 values were observed in patients with non-toxic nodular goiter compared with healthy children. PMID:11085183

Bossowski, A; Urban, M; Gardziejczyk, M; Kitszel, A; Rogowski, F; Sobotko, J

2000-01-01

199

Adhesions  

MedlinePLUS

... any problems. But when they partly or completely block the intestines, they cause symptoms such as Severe abdominal pain or cramping Vomiting Bloating An inability to pass gas Constipation Adhesions can ...

200

Gene structure of rat testicular cell adhesion molecule 1 (TCAM-1), and its physical linkage to genes coding for the growth hormone and BAF60b, a component of SWI/SNF complexes.  

PubMed

In the +9.7 to +21.7kb downstream region from the transcriptional start site of the rat growth hormone (GH) gene, a gene specifically expressed in the testis was found to have reverse transcriptional orientation to the GH gene. Its exon comprised 2693 bases encoded a protein having 548 amino acids (60479Da). The amino acid sequence of the testis-specific protein resembled that of the intercellular adhesion molecules (ICAM) 1 and 3. The gene was thus given the name testicular adhesion molecule (TCAM) 1 gene. The TCAM-1 gene was found to be 12041 bases with eight exons. Although exon 1 was noncoding, the remaining seven exons corresponded to the domains coding for the signal sequence, five immunoglobulin (Ig) domains, and the transmembrane plus cytoplasmic domain. The organization of TCAM-1 gene was shown to be the same as that of the ICAM-1 gene. The polyadenylation site of TCAM-1 gene was located 7.6kb downstream of that of the GH gene, whereas the 5' end of TCAM-1 gene was separated 5.9kb from that of the gene coding for BAF60b, a component of SWI/SNF complexes known as the chromatin remodeling factor. Six genes were thus mapped in the following order in the 88kb region of the rat GH locus: Na-channel (5' to 3')-B29/Ig-beta (5' to 3')-GH (5' to 3')-TCAM-1 (3' to 5')-BAF60b (5' to 3')-SUG/p45 (3' to 5'). PMID:9889334

Ono, M; Nomoto, K; Nakazato, S

1999-01-01

201

Reduced antigen-presenting function of human Epstein-Barr virus (EBV)-B cells and monocytes after UVB radiation is accompanied by decreased expression of B7, intercellular adhesion molecule-1 (ICAM-1) and LFA-3.  

PubMed Central

In this study, the effect of ultraviolet-B (UVB) radiation on antigen-presenting function was studied, to investigate whether antigen-presenting cells (APC) are inhibited by UVB through a common mechanism. Two types of human APC were used: EBV-B cells and monocytes, and these were irradiated in vitro with single low doses of UVB (range 0-200 J/m2). Irradiation of EBV-B cells or monocytes resulted in similar dose-dependent reduction in APC function, when determined by the allogeneic mixed leucocyte reaction (MLR) or Candida albicans- or tetanus toxoid-specific T cell response. Our study shows that the reduced APC function was not likely to be caused by alterations in antigen processing or cytokine production. However, UVB-irradiated APC displayed marked changes in adhesion molecule expression. Irradiated EBV-B cells showed reduced expression of ICAM-1 (30%), LFA-3 (25%) and B7-1 (35%), while expression of HLA-DR, CD19 and LFA-1 was not affected. UVB irradiation of monocytes did result in reduction in the expression of HLA-DR (30%), LFA-3 (40%), ICAM-1 (65%) AND B7-1 and B7-3 (90%), but had no effect on CD14, LFA-1 and ICAM-3 expression. Addition of non-irradiated cells (but not the supernatant of these cells) or CD28 antibodies partly restored T cell activation, indicating that UVB-induced reduction in APC function is at least partly mediated via impairment of co-stimulatory molecule expression.

Kremer, I B; Bos, J D; Teunissen, B M

1995-01-01

202

Intercellular adhesion molecules (ICAMs) and spermatogenesis  

PubMed Central

BACKGROUND During the seminiferous epithelial cycle, restructuring takes places at the Sertoli–Sertoli and Sertoli–germ cell interface to accommodate spermatogonia/spermatogonial stem cell renewal via mitosis, cell cycle progression and meiosis, spermiogenesis and spermiation since developing germ cells, in particular spermatids, move ‘up and down’ the seminiferous epithelium. Furthermore, preleptotene spermatocytes differentiated from type B spermatogonia residing at the basal compartment must traverse the blood–testis barrier (BTB) to enter the adluminal compartment to prepare for meiosis at Stage VIII of the epithelial cycle, a process also accompanied by the release of sperm at spermiation. These cellular events that take place at the opposite ends of the epithelium are co-ordinated by a functional axis designated the apical ectoplasmic specialization (ES)—BTB—basement membrane. However, the regulatory molecules that co-ordinate cellular events in this axis are not known. METHODS Literature was searched at http://www.pubmed.org and http://scholar.google.com to identify published findings regarding intercellular adhesion molecules (ICAMs) and the regulation of this axis. RESULTS Members of the ICAM family, namely ICAM-1 and ICAM-2, and the biologically active soluble ICAM-1 (sICAM-1) are the likely regulatory molecules that co-ordinate these events. sICAM-1 and ICAM-1 have antagonistic effects on the Sertoli cell tight junction-permeability barrier, involved in Sertoli cell BTB restructuring, whereas ICAM-2 is restricted to the apical ES, regulating spermatid adhesion during the epithelial cycle. Studies in other epithelia/endothelia on the role of the ICAM family in regulating cell movement are discussed and this information has been evaluated and integrated into studies of these proteins in the testis to create a hypothetical model, depicting how ICAMs regulate junction restructuring events during spermatogenesis. CONCLUSIONS ICAMs are crucial regulatory molecules of spermatogenesis. The proposed hypothetical model serves as a framework in designing functional experiments for future studies.

Xiao, Xiang; Mruk, Dolores D.; Cheng, C. Yan

2013-01-01

203

Soluble E-selectin, other markers of inflammation and disease severity in children with atopic dermatitis  

Microsoft Academic Search

E-selectin, P-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) are membrane-bound adhesion molecules which mediate the attachment of leucocytes to endothelial cells. These molecules are preferentially expressed on activated endothelium. The soluble forms of these molecules (sE-selectin, sP-selectin, sICAM-1 and sVCAM-1) are present in the circulation as a result of shedding. Some of the soluble adhesion molecules

A. Wolkerstorfer; M. P. Laan; H. F. J. Savelkoul; H. J. Neijens; P. G. Mulder; A. M. Oudesluys-Murphy; R. N. Sukhai; A. P. Oranje

1998-01-01

204

Reduction of the ST6 ?-Galactosamide ?-2,6-Sialyltransferase 1 (ST6GAL1)-catalyzed Sialylation of Nectin-like Molecule 2/Cell Adhesion Molecule 1 and Enhancement of ErbB2/ErbB3 Signaling by MicroRNA-199a*  

PubMed Central

Nectin-like molecule 2 (Necl-2)/cell adhesion molecule 1 (CADM1) is shown to be down-regulated by the promoter hypermethylation and/or loss of heterozygosity at chromosome 11q23.2 in many types of cancers, including lung and breast cancers, and is proposed to serve as a tumor suppressor. However, the incidence of these epigenetic and genetic abnormalities of Necl-2 is 30–60% in these cancers, and other mechanisms for the suppression of Necl-2 are presumed to be present. We previously showed that Necl-2 interacts in cis with ErbB3 and suppresses the heregulin (HRG)-induced ErbB2/ErbB3 signaling for cell movement and death. We studied here the relationship between Necl-2 and microRNA-199a (miR-199a) that is up-regulated or down-regulated in a variety of cancers. miR-199a did not directly target the Necl-2 mRNA or affect its mRNA level in human lung cancer A549 cells and human embryonic kidney HEK293 cells. Necl-2 was at least sialylated by the sialyltransferase ST6 ?-galactosamide ?-2,6-sialyltransferase 1 (ST6GAL1). miR-199a targeted ST6GAL1 and reduced both the sialylation and the protein level of Necl-2. In addition, miR-199a enhanced the HRG-induced ErbB2/ErbB3 signaling. These results indicate that the suppressive role of Necl-2 in the HRG-induced ErbB2/ErbB3 signaling is regulated by miR-199a at least through the reduction of the ST6GAL1-catalyzed sialylation of Necl-2 and/or through the reduction of the protein level of Necl-2 presumably by the protein degradation.

Minami, Akihiro; Shimono, Yohei; Mizutani, Kiyohito; Nobutani, Kentaro; Momose, Kenji; Azuma, Takeshi; Takai, Yoshimi

2013-01-01

205

Weight loss and vascular inflammatory markers in overweight women with and without polycystic ovary syndrome.  

PubMed

Polycystic ovary syndrome (PCOS) is associated with increased cardiovascular disease risk. The effect of weight loss on the vascular inflammatory markers plasminogen activator inhibitor-1 (PAI-1), asymmetric dimethylarginine (ADMA), soluble vascular cell adhesion molecule-1 (sVCAM-1) and intracellular adhesion molecule-1 (sICAM-1) is unknown. Overweight women with (n=14) and without (n=13) PCOS of comparable age and body mass index undertook an 8-week weight-loss programme. Women with PCOS had elevated PAI-1, sVCAM-1 and sICAM-1 before and after weight loss compared with the controls. For all women, sVCAM-1 (P=0.026) and sICAM-1 (P=0.04) decreased with weight loss. Women with PCOS have elevated inflammatory markers, which are partially reduced by weight loss. PMID:22995747

Moran, Lisa J; Noakes, Manny; Wittert, Gary A; Clifton, Peter M; Norman, Robert J

2012-11-01

206

Combined measurement of soluble and cellular ICAM-1 among children with Plasmodium falciparum malaria in Uganda  

PubMed Central

Background Intercellular adhesion molecule-1 (ICAM-1) is a cytoadhesion molecule implicated in the pathogenesis of Plasmodium falciparum malaria. Elevated levels of soluble ICAM-1 (sICAM-1) have previously been reported with increased malaria disease severity. However, studies have not yet examined both sICAM-1 concentrations and monocyte ICAM-1 expression in the same cohort of patients. To better understand the relationship of soluble and cellular ICAM-1 measurements in malaria, both monocyte ICAM-1 expression and sICAM-1 concentration were measured in children with P. falciparum infection exhibiting a spectrum of clinical severity. Methods Samples were analysed from 160 children, aged 0.5 to 10.8 years, with documented P. falciparum malaria in Kampala, Uganda. The patients belonged to one of three pre-study defined groups: uncomplicated malaria (UM), severe non-fatal malaria (SM-s), and fatal malaria (SM-f). Subset analysis was done on those with cerebral malaria (CM) or severe malaria anaemia (SMA). Monocyte ICAM-1 was measured by flow cytometry. sICAM-1 was measured by enzyme immunoassay. Results Both sICAM-1 and monocyte cell-surface ICAM-1 followed a log-normal distribution. Median sICAM-1 concentrations increased with greater severity-of-illness: 279 ng/mL (UM), 462 ng/mL (SM-s), and 586 ng/mL (SM-f), p < 0.0001. sICAM-1 levels were not statistically different among children with CM compared to SMA. Monocyte ICAM-1 expression was significantly higher in cases of UM compared with SM-s or SM-f (p < 0.001) and was higher among the subset of patients with CM compared with SMA, p < 0.0014. The combination of sICAM-1 and cellular ICAM-1 identified distinct categories of patients (UM with low sICAM-1 and higher monocyte ICAM-1, CM with both sICAM-1 and monocyte ICAM-1 high, and SMA with sICAM-1 high but monocyte ICAM-1 low). Conclusion In this cohort of children with P. falciparum malaria, sICAM-1 levels were associated with severity-of-illness. Patients with UM had higher monocyte ICAM-1 expression consistent with a role for monocyte ICAM-1 in immune clearance during non-severe malaria. Among the subsets of patients with either SMA or CM, monocyte ICAM-1 levels were higher in CM, consistent with the role of ICAM-1 as a marker of cytoadhesion. Categories of disease in pediatric malaria may exhibit specific combinations of soluble and cellular ICAM-1 expression.

2010-01-01

207

Intercellular adhesion molecule-1 is an endothelial cell adhesion receptor for Plasmodium falciparum  

Microsoft Academic Search

THE primary event in the pathogenesis of severe malaria in Plasmodium falciparum infection is thought fo be adherence of trophozoite- and schizont-infected erythrocytes to capillary endothelium1, a process called sequestration. Identifying the endothelial molecules used as receptors is an essential step in understanding this disease process. Recent work implicates the membrane glycoprotein CD36 (platelet glycoprotein IV; refs 2-5) and the

A. R. Berendt; D. L. Simmons; J. Tansey; C. I. Newbold; K. Marsh

1989-01-01

208

The influence of garlic ( Allium sativum) extract on interleukin 1 ?-induced expression of endothelial intercellular adhesion molecule-1 and vascular cell adhesion molecule-1  

Microsoft Academic Search

Inflammation plays an important role in both the initiation of atherosclerosis and development of atherothrombotic events. The adherence of leukocytes\\/monocytes to the endothelium is an early event in atherogenesis. Phytotherapeutica as garlic and garlic extracts were shown to have beneficial modulating effects in patients with atherosclerotic disease. The aim of this study was to evaluate in vitro the influence of

F. Rassoul; J. Salvetter; D. Reissig; W. Schneider; J. Thiery; V. Richter

2006-01-01

209

148 Levels of F VCAM and ICAM in Patients With Allergic Rhino-Conjunctivitis and H1 Antihistamines  

PubMed Central

Background Soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular adhesion molecule-1 (sVCAM-1) play and important role in eosinophilic inflammation in allergic rhino-conjunctivitis (ARC). ICAM-1 and VCAM-1 have been identified as key molecules in allergic inflammatory diseases and in a few studies there was an increased value of those molecules in patients with allergic rhinitis. Treatment with H1 antihistamines is known to improve symptoms in allergic rhinitis and in vitro reduces the levels of adhesion molecules. Object To evaluate serum levels of sICAM-1 and sVCAM-1 in pts with ARC to grass pollen and the response to different antihistamines. Methods 50 pts with allergic rhino-conjunctivitis to grass pollen were evaluated regarding levels of sICAM-1 and sVCAM-1. The serum sICAM-1 and sVCAM-1 were evaluated during pollen season before and after antihistaminic terapy. Quantikine R&D System was used. Normal mean values in healthy volunteers were 208 ng/mL for sICAM and 557 ng/mL for sVCAM-1. 54% of pts were women and 88% from urban area. Results Mean levels of sICAM-1 and sVCAM-1 were elevated before therapy of the pts compared with mean values in healthy subjects (235 ng/mL vs 208 ng/mL for sICAM and 966 ng/mL vs 557 ng/mL for sVCAM. 42% of pts received desloratadine therapy and 58% of them received levocetirizine. In both treated groups’ levels of sICAM-1 and sVCAM-1 increased after one month of antihistaminic therapy but no statistical significance. Was obtained: in desloratadine group sICAM-1 (P = 0.066) and sVCAM-1 (P = 0.096); in levocetirizine group sICAM-1 (P = 0.681) and sVCAM-1 (P = 0.4060. Patients with high levels of sICAM-1 and sVCAM-1 at the tended to have increased sICAM-1 and sVCAM-1 levels at one month (P = 0.000). No statistical difference was obtained between the 2 treated groups after one month regarding the levels of sICAM-1 and sVCAM-1. Conclusions In patients with allergic rhino-conjunctivitis to grass pollen levels of sICAM-1 and sVCAM-1 are higher than in healthy subjects. Levels of sICAM-1 and sVCAM-1 in serum tend to increase during pollen season despite antihistaminic therapy.

Bujor, Ioana Adriana; Corina, Bocsan Ioana; Deleanu, Diana

2012-01-01

210

Effect of Soy Nuts on Adhesion Molecules and Markers of Inflammation in Hypertensive and Normotensive Postmenopausal Women  

PubMed Central

Recently, we showed that substituting soy nuts for non-soy protein in a therapeutic lifestyle change (TLC) diet lowered systolic and diastolic blood pressure 9.9% and 6.8%, respectively, in hypertensive postmenopausal women and 5.2% and 2.9%, respectively, in normotensive postmenopausal women. To examine mechanisms for these reductions, we measured markers of inflammation including soluble vascular cell adhesion molecule (sVCAM-1), soluble intercellular adhesion molecule (sICAM-1), C-reactive protein (CRP), interleukin-6 (IL-6) and matrix metalloproteinase-9 (MMP-9). Sixty healthy postmenopausal women (48 normotensive and 12 hypertensive) were randomized in a crossover design to a TLC diet alone or a TLC diet in which one-half cup soy nuts (25 g soy protein and 101 mg aglycone isoflavones) replaced 25 g of non-soy protein daily. Each diet was followed for 8 weeks. Compared to the TLC diet alone, levels of sVCAM-1 were significantly lower on the soy diet in hypertensive women (623.6±153.8 ng/ml versus 553.8±114.4 ng/ml, respectively, p=0.003) whereas no significant differences were observed in normotensive women. Soy nuts were associated with a trend toward reduction in CRP in normotensive women. No effect on levels of sICAM-1, IL-6 or MMP-9 was observed. In conclusion, the reduction in sVCAM-1 with soy nuts in hypertensive women suggests an improvement in endothelial function which may reflect an overall improvement in the underlying inflammatory process underlying atherosclerosis.

Nasca, Melita M.; Zhou, Jin-Rong; Welty, Francine K.

2011-01-01

211

Soluble adhesion molecules and unstable coronary artery disease  

Microsoft Academic Search

Leukocyte adhesion and transendothelial migration, prerequisites in the development of atherosclerosis, are largely mediated by adhesion molecules. In addition, unstable coronary syndromes usually involve platelet activation and thrombus formation at the site of atherosclerotic plaque. Therefore, we compared plasma levels of soluble P-selectin, a measurement of platelet activation, as well as E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion

Crawford Parker; Joseph A. Vita; Jane E. Freedman

2001-01-01

212

Inhibition of activation of human peripheral blood eosinophils by Y-24180, an antagonist to platelet-activating factor receptor  

Microsoft Academic Search

We examined the effects of Y-24180, a potent and long-acting antagonist to platelet-activating factor (PAF) receptor, on the PAF- or leukotriene B4 (LTB4)-induced activation of eosinophils using human peripheral blood in vitro. As activation markers, CD11b expression level and soluble intercellular adhesion molecule-1 (sICAM-1)-binding activity were analyzed by flow cytometry. Y-24180 significantly inhibited PAF-induced increase in the ratio of strongly

Hirotsugu Komatsu; Mariko Amano; Shuji Yamaguchi; Kunio Sugahara

1999-01-01

213

Cerebral malaria among children from central Sudan and intercellular adhesion molecule-1 mutation  

Microsoft Academic Search

The study was carried out to investigate the distribution of cerebral malaria in central region and to identify ICAM-1 alleles and genotypes frequency in Sudanese population in the region. Fifty children with cerebral malaria and 50 age- and sex-matched healthy controls with no history of cerebral malaria were enrolled in the study. The highest incidencts of cerebral malaria were found

Mohammed S. Zaroog; Ahmed EL Tahir; Adil Mergani; ELfatih Hashim; Mohamed Gumma; Ali Babkier Haboor; Nase ELdin; M. A. Elwali

214

Maternal Serum Levels of VCAM-1, ICAM-1 and E-selectin in Preeclampsia  

PubMed Central

Endothelial dysfunction is thought to be a central pathogenic feature in preeclampsia on the basis of elevated adhesion molecules. The aim of the present study was to compare the levels of soluble vascular cell adhesion molecule-1 (sVCAM-1), intercellular adhesion molecule-1 (sICAM-1) and E-selectin (sE-selectin) in sera of normal and preeclamptic pregnancies. We studied the serum levels of sVCAM-1, sICAM-1 and sE-selectin in normal pregnant women (n=63), mild preeclampsia (n=33) and severe preeclampsia (n=82). Concentrations of soluble adhesion molecules were determined with enzyme-linked immunoassay (ELISA). Serum concentrations of sVCAM-1 were significantly higher in both mild (p=0.004) and severe preeclampsia (p=0.000) than normal pregnancy. There were also significant differences in sVCAM-1 levels between mild and severe preeclampsia (p=0.002). sICAM-1 levels of severe preeclampsia were statistically different from those of normal pregnancy (p=0.038). Levels of sE-selectin were elevated in both mild (p=0.011) and severe preeclampsia (p=0.000) compared to normal pregnancy, but no statistical difference between the mild and severe preeclampsia (p=0.345). These results suggest that all three soluble adhesion molecules are increased in severe preeclampsia, and sVCAM-1 among them may be useful in predicting the severity of preeclampsia.

Kim, Shin-Young; Yang, Jae Hyug; Kim, Moon-Young; Ahn, Hyun-Kyong; Lim, Ha-Jung; Shin, Joong-Sik; Woo, Hyuk-Jun; Park, So-Yeon; Kim, Young-Mi; Kim, Jin-Woo; Cho, Eun Hee

2004-01-01

215

Serum soluble markers in the evaluation of treatment in human visceral leishmaniasis.  

PubMed Central

Visceral leishmaniasis (VL) has a fatal course if not properly treated. Recovery from VL is linked to cellular immune response. Unresponsiveness to antimonial therapy reinforces the importance of determining parameters for treatment assessment. We analysed the pre- and post-treatment serum levels of soluble CD4 (sCD4), sCD8, sIL-2R, soluble intercellular adhesion molecule-1 (sICAM-1) and neopterin in groups of VL patients either responsive or not to standard antimonial therapy. Pretreatment serum levels of all markers except for sICAM-1 were significantly higher in VL patients than in healthy subjects from the same area (P < 0.05). sICAM-1 levels were similar in healthy controls and in VL patients refractory to antimonial therapy (P = 0.25), but significantly higher in patients responsive to treatment (P = 0.02). The comparison of pre- and post-treatment concentrations showed that all markers, except sCD4 and sICAM-1, presented a significant fall (P < 0.05) in patients responsive to antimonial therapy. However, only neopterin presented with levels compatible with those of healthy subjects at the end of treatment (P = 0.30). In refractory patients sICAM-1 presented with post-treatment levels significantly higher than the pretreatment determinations (P = 0.03), while sCD4 experienced a significant drop (P = 0.01). All markers displayed clearly distinct behaviour according to the patient's response to therapy. This makes all soluble molecules studied suitable for use as indicators of antimonial therapy response. Additionally the comparison of pretreatment levels of the markers between responders and refractory patients to antimonial therapy showed that serum concentrations of sIL-2R and sICAM-1 significantly differed among these two groups (P = 0.02 in each case), suggesting that they may be used in future as predictors of antimonial therapy response.

Schriefer, A; Barral, A; Carvalho, E M; Barral-Netto, M

1995-01-01

216

Serum levels of adhesion molecules and thrombomodulin as indicators of vascular injury in severe Plasmodium falciparum malaria  

Microsoft Academic Search

Severe Plasmodium falciparum malaria is characterized by multiple organ involvment due to sequestration of infected erythrocytes in small vessels. Endothelial cell adhesion molecules play an important role in this interaction. During the course of a severe cerebral P. falciparum malaria infection we found very markedly elevated levels of the soluble adhesion molecules intercellular adhesion molecule-1, E-selectin, and vascular cell adhesion

M. W. J. Boehme; E. Werle; B. Kommerell; U. Raeth

1994-01-01

217

Adhesion molecules and transplantation.  

PubMed Central

OBJECTIVE: Accessory adhesion molecules are thought to influence the first interaction between host leukocytes and graft vascular endothelial cells. Their role in transplantation is reviewed. SUMMARY: Adhesion molecules have been divided into three major families: the selectins, the integrins, and the immunoglobulin superfamily. Selectins are small proteins that mediate the first contact between stimulated endothelial cells and leukocytes. Integrins interact with cytoskeletal components of cells, presumably coordinating extracellular stimuli with cytoskeleton dependent actions, such as motility, shape change, and phagocytic responses. Members of the immunoglobulin superfamily are structurally homologous, although they do not necessarily share similar functions. They are involved in T-cell proliferation and intracellular events. METHODS: Various groups of investigators have studied the influence and expression of adhesion molecules following transplantation. The authors of this article have reviewed and summarized the available literature. RESULTS: Many different adhesion molecules are up-regulated during the rejection event. Treatment of transplant recipients with monoclonal antibodies against accessory molecules, such as leukocyte function associated antigen 1 (LFA-1) and intercellular adhesion molecule 1 (ICAM-1), has resulted in either a prolongation of transplant survival or the induction of tolerance in some models. Other interventions are under study. CONCLUSION: By mediating the initial leukocyte/endothelial cell interactions, adhesion molecules may play an important role in graft rejection, mediation of infiltration into the graft, and dissemination of the antigenic message to the lymphoid tissues of the host. Future studies will have to deal not only with conceptualizing their function and mechanisms of action, but also with manipulating their interrelationships to the benefit of the graft recipient.

Heemann, U W; Tullius, S G; Azuma, H; Kupiec-Weglinsky, J; Tilney, N L

1994-01-01

218

Circulating adhesion molecules after short-term exposure to particulate matter among welders  

PubMed Central

Background Studies from several countries indicate that welders experience increased risk of mortality and morbidity from ischaemic heart disease. Although the underlying mechanisms are unclear, vascular responses to particulate matter contained in welding fumes may play a role. To investigate this, we studied the acute effects of welding fume exposure on the endothelial component of vascular function, as measured by circulating adhesion molecules involved in leukocyte adhesion (sICAM-1 and sVCAM-1) and coagulation (vWF). Methods A panel of 26 male welders was studied repeatedly across a 6 h work-shift on a high exposure welding day and/or a low exposure non-welding day. Personal PM2.5 exposure was measured throughout the work-shift. Blood samples were collected in the morning (baseline) prior to the exposure period, immediately after the exposure period, and the following morning. To account for the repeated measurements, we used linear mixed models to evaluate the effects of welding (binary) and PM2.5 (continuous) exposure on each blood marker, adjusting for baseline blood marker concentration, smoking, age and time of day. Results Welding and PM2.5 exposure were significantly associated with a decrease in sVCAM-1 in the afternoon and the following morning and an increase in vWF in the afternoon. Conclusions The data suggest that welding and short-term occupational exposure to PM2.5 may acutely affect the endothelial component of vascular function.

Fang, S C; Eisen, E A; Cavallari, J M; Mittleman, M A; Christiani, D C

2011-01-01

219

Denture Adhesives  

MedlinePLUS

... denture adhesives. Over time, shrinkage in the bone structure in the mouth causes dentures to gradually become ... increase in bone loss. The FDA recommends that consumers of denture adhesive products: Follow the instructions provided ...

220

Impact of static cold storage VS hypothermic machine preservation on ischemic kidney graft: inflammatory cytokines and adhesion molecules as markers of ischemia/reperfusion tissue damage. Our preliminary results.  

PubMed

At the present time, deceased heart-beating donor kidney allografts are usually stored cold. Extended-criteria donor (ECD) grafts show higher sensitivity to ischemia-reperfusion damage than standard kidneys. The increasing use of marginal organs in clinical transplantation urgently requires a more effective preservation system. Pulsatile hypothermic machine perfusion has shown major advantages over static cold storage in terms of reduced organ injury during preservation and improved early graft function. This preliminary study aims to compare pulsatile hypothermic machine perfusion and static cold storage of kidney allografts, outlining differences in the levels of early inflammatory cytokines (TNF-?, IL-2 and IL-1?) and soluble intracellular adhesion molecule (sICAM-1) in perfusion and preservation liquid. PMID:24380541

Tozzi, Matteo; Franchin, Marco; Soldini, Gabriele; Ietto, Giuseppe; Chiappa, Corrado; Maritan, Emanuele; Villa, Francesca; Carcano, Giulio; Dionigi, Renzo

2013-01-01

221

Association of ophthalmic complications in patients with sulfur mustard induced mild ocular complications and serum soluble adhesion molecules: Sardasht-Iran Cohort Study.  

PubMed

The aim of this study was to evaluate possible association between ophthalmic complications in sulfur mustard (SM) exposed patients with mild ocular injuries and serum soluble adhesion molecules. Serum levels of sICAM-1, sL-selectin, sP-selectin and sE-selectin in 367 SM-exposed individuals with or without eye injuries were checked and compared with 128 unexposed controls. All participants underwent ocular examinations. Serum sICAM-1 level in SM exposed with blurred vision, was significantly (p=0.021) higher than in SM exposed with no blurred vision. Serum sL-selectin level was significantly (p=0.024) higher in SM exposed with photophobia than SM exposed with no photophobia. Serum P-selectin level in exposed without any slit lamp findings was significantly (p=0.003) lower than the matched control groups. Similar finding was seen in exposed group without ocular problem compared with the control groups. Serum sE-selectin level in exposed with normal ocular condition except for photophobia and blurred vision was significantly (p<0.05) higher than the matched controls. Serum E-selectin level in exposed with photophobia condition was significantly (p=0.047) higher than the control group with photophobia. In conclusion it seems that the changes in the E- and P-selectins is a regulatory mechanism for inhibition of SM induced ocular problems, although the local levels are more important and further investigations required in more severe ocular problems in SM exposed patients. PMID:23370300

Ghasemi, Hassan; Yaraee, Roya; Hassan, Zuhair Mohammad; Faghihzadeh, Soghrat; Soroush, Mohammad-Reza; Pourfarzam, Shahriar; Ebtekar, Massoumeh; Babaei, Mahmoud; Moaiedmohseni, Sakine; Naghizadeh, Mohammad-Mehdi; Askari, Nayere; Ghazanfari, Tooba

2013-11-01

222

Kinetics of immunological parameters in patients with malignant melanoma treated with hyperthermic isolated limb perfusion.  

PubMed

Kinetics of immunological parameters such as natural killer (NK) cell activity and tritium-thymidine uptake rate of T lymphocytes by phytohemagglutinin stimulation were investigated using peripheral leukocyte fractions of melanoma patients treated with hyperthermic isolated limb perfusion (HILP). Also, serum concentrations of soluble intercellular adhesion molecule-1 (sICAM-1) were quantified during and after HILP. It was found that NK cell activity was augmented during HILP, and T lymphocyte function was stimulated 24 h and 1 week after HILP with statistical significance. NK cell activities in the cells isolated from perfused and non-perfused circulations were equally augmented during HILP in two patients examined. Serum concentrations of sICAM-1 in the patients who received HILP also increased 24 h or even 1 week after HILP. The stimulation of these immune competent cells and upregulation of sICAM-1 by HILP were independent of the stages of melanoma patients at the time of HILP or the doses of agents which were used for the infusion during HILP. The origin of cells which shed sICAM-1 into the serum of the patients who received HILP remains to be further investigated. PMID:9186806

Nakayama, J; Nakao, T; Mashino, T; Nagae, S; Hori, Y; Mayumi, H; Tominaga, R; Yasui, H; Matsuda, K; Takahashi, S

1997-05-01

223

Multiple antioxidants and L-arginine modulate inflammation and dyslipidemia in chronic renal failure rats.  

PubMed

The kidney is an important source of L-arginine, the endogenous precursor of nitric oxide (NO). Surgical problems requiring extensive renal mass reduction (RMR) decrease renal NO production, leading to multiple hemodynamic and homeostatic disorders manifested by hypertension, oxidative stress, and increased inflammatory cytokines. Using the RMR model of chronic renal failure (CRF), we assessed the effects of twelve weeks' administration of L-arginine and/or a mixture of antioxidants (L-carnitine, catechin, vitamins E and C) on plasma cytokines, soluble intercellular adhesion molecule-1 (sICAM-1), nitrate and nitrites (NO(2)/NO(3)), lipid profile, blood pressure, and renal function. CRF rats showed increased plasma IL-1 alpha, IL1-beta, IL-6, TNF-alpha, and sICAM-1 levels and decreased anti-inflammatory cytokines IL-4 and 10 levels, hypertension, and dyslipidemia. L-arginine treatment improved kidney functions, decreased systolic blood pressure, and decreased inflammatory cytokines levels. Antioxidants administration decreased inflammatory cytokines and sICAM-1 levels and increased IL-4 levels. Combined use of both L-arginine and the antioxidant mixture were very effective in their tendency to recover normal values of kidney functions, plasma cytokines, sICAM-1, blood pressure, NO(2)/NO(3), cholesterol, and triglycerides concentrations. Indeed, the effects of L-arginine and the antioxidants on the reduction of proinflammatory cytokines may open new perspectives in the treatment of uremia. PMID:20199183

Korish, Aida A

2010-01-01

224

Temporal Patterns of Soluble Adhesion Molecules in Cerebrospinal Fluid and Plasma in Patients with the Acute Brain Infraction  

PubMed Central

The aim of this study was to define concentration changes of soluble adhesion molecules (sICAM-1, sVCAM-1 and sE-Selectin) in cerebrospinal fluid and plasma, as well as, number of peripheral blood leukocytes and the albumin coefficient in the patients with the acute brain infarction. We also, analyzed the correlation between the measured levels, the infarct volume and the degree of neurological and the functional deficit. The study included 50 patients with the acute cerebral infarction and the control group consisted of 16 patients, age and sex matched. Obtained results showed significant increase in number of leukocytes, the albumin coefficient and the level of soluble adhesion molecules within the first seven days in patients. The highest values of measured parameters were noted within the third and the fourth day after the insult, which is the suggested period of maximal intensity of inflammatory reactions. Significant correlation was found between measured parameters and the infarct volume, the degree of neurological and the functional deficit. The results suggest that investigated parameters in CSF and blood represent a dynamic index of inflammatory events as one of the fundametal mechanisms responsible for neuron damage during acute phase of brain infarction.

Selakovic, Vesna; Raicevic, Ranko; Radenovic, Lidija

2009-01-01

225

Intrauterine Adhesions  

MedlinePLUS

... the cavity of the uterus. Dilatation and curettage (D&C) is a common outpatient surgical procedure during which ... are emptied. Intrauterine adhesions may form following a D&C performed for pregnancy complications such as uterine bleeding ...

226

Abdominal Adhesions  

MedlinePLUS

... cavity to stick together. What is the abdominal cavity? The abdominal cavity is the internal area of the body between ... adhesions cause tissues and organs in the abdominal cavity to stick together. • Abdominal surgery is the most ...

227

Abdominal Adhesions  

MedlinePLUS

... tissues and organs. [ Top ] What is the abdominal cavity? The abdominal cavity is the internal area of the body between ... adhesions cause tissues and organs in the abdominal cavity to stick together. Abdominal surgery is the most ...

228

Effects of baicalein isolated from Scutellaria baicalensis on interleukin 1 ?- and tumor necrosis factor ?-induced adhesion molecule expression in cultured human umbilical vein endothelial cells  

Microsoft Academic Search

We examined the effects of nine flavonoids isolated from Scutellariae radix on interleukin-1? (IL-1?)- and tumor necrosis factor-? (TNF-?)- induced adhesion molecule expression in cultured human umbilical vein endothelial cells (HUVECs). Among them, we found that baicalein (5,6,7-trihydroxy flavone) dose-dependently inhibited IL-1? and TNF-?-induced endothelial leukocyte adhesion molecule-1 (ELAM-1) and intercellular adhesion molecule-1 (ICAM-1) expressions. Its 50% inhibitory concentrations (IC50)

Yoshiyuki Kimura; Nobutoshi Matsushita; Hiromichi Okuda

1997-01-01

229

Tumor necrosis factor-? up-regulates the expression of CCL2 and adhesion molecules of human proximal tubular epithelial cells through MAPK signaling pathways  

Microsoft Academic Search

Both circulating and urinary tumor necrosis factor (TNF)-? levels have been shown to increase in inflammatory chronic kidney diseases and TNF-? can induce secretion of other inflammatory mediators from many cell types. Chemokine, mononuclear chemoattractant protein-1 (CCL2\\/MCP-1), and cell surface adhesion molecules, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), in renal proximal tubular epithelial cells (PTEC) are

Amy Wing Yin Ho; Chun Kwok Wong; Christopher Wai Kei Lam

2008-01-01

230

The Associrlation of the Seaum Cellular Adhesion Molecule Level with Tytepe One Diabetes Aetinotathy  

Microsoft Academic Search

Objective Tobetter understand potential associations of circulating adhesionmolecules(cAMs) with diabetic retinopathy(DR) ,circu2 lation serum concentrations of intercellular adhesion molecule - 1 ( cICAM - 1) was determined in patients with insulin - dependent diabetic mellitus ( IDDM n = 32) presenting with varying degrees of metabolic control and status of diabetic retinopathy. Methods The serum levels of circulative intercellular adhesion

HAN Mei

2005-01-01

231

Defective Expression of Adhesion Molecules on Human Bladder Tumour and Human Tumour Cell Lines  

Microsoft Academic Search

The pattern of expression of cell adhesion molecules, i.e., leucocyte function associated antigen 3 (LFA-3) and intercellular adhesion molecule 1 (ICAM-1) on human bladder tumour biopsy specimens was investigated. Attempts were also made to study the pattern of induction of these molecules by established human cell lines in response to cytokines. The results indicated that 15 of 25 tumour biopsy

A. M. E. Nouri; R. F. Hussain; A. V. L. Dos Santos; R. T. D. Oliver

1996-01-01

232

Polyimide adhesives  

NASA Technical Reports Server (NTRS)

A process of preparing aromatic polyamide-acids for use as adhesives is described. An equimolar quantity of an aromatic dianhydride is added to a stirred solution of an aromatic diamine in a water or alcohol-miscible ether solvent to obtain a viscous polymer solution. The polymeric-acid intermediate polymer does not become insoluble but directly forms a smooth viscous polymer solution. These polyamic-acid polymers are converted, by heating in the range of 200-300 C and with pressure, to form polyimides with excellent adhesive properties.

Progar, D. J.; Bell, V. L.; Saintclair, T. L. (inventors)

1974-01-01

233

Increased soluble endothelial adhesion molecules in rheumatoid arthritis correlate with circulating cytokines and depletion of CD45RO+ T-lymphocytes from blood stream.  

PubMed

Endothelial cells express adhesion molecules and release free forms (e.g., sELAM-1, sGMP-140, sICAM-1 and sVCAM-1). Compared with controls, the serum levels of these soluble adhesion molecules (SAM) were significantly increased in patients with rheumatoid arthritis. We investigated whether this was associated with the circulating cytokines and changes in peripheral blood T-lymphocyte (T-PBL) subsets. In healthy subjects, sELAM-1 correlated with the serum levels of Il-1 beta, Il-1 receptor antagonist (Il-1RA) and Il-6, while sGMP-140 was associated with Il-8, and sVCAM-1 was related to Il-7 and Il-8. Thus, already in controls, relations exist between the levels of SAM and circulating cytokines. The rheumatoid arthritis patients with low and high serum levels of IgA- and/or IgM-rheumatoid factors (RF) were separately analyzed. They have different cytokine profiles and showed distinct correlations. In patients with low RF, sGMP-140 and sVCAM-1 correlated with Il-1 beta, while sICAM-1 was associated with Il-7 and TNF-alpha. In patients with high RF, sELAM-1 correlated with Il-1RA, and sGMP-140 was associated with many cytokines (e.g., GM-CSF, MIP-1 alpha and TNF-alpha). In addition, lymphopenia (less than 1000 lymphocytes/microliters) was shown in 30% of the patients, and 20% (mostly with low RF levels) had reduced levels of "primed" CD45RO+ cells among T-PBL. In controls, cytokines (Il-7, Il-8 and GM-CSF), but not SAM, were associated with less CD45RO+ T-PBL. In patients with low RF only, sGMP-140 and sELAM-1 correlated with the depletion of "primed" CD4+ and CD8+ T-PBL respectively. In such patients, Il-1 beta and GM-CSF also correlated with less CD8+, CD45RO+ T-PBL. Thus, particularly in patients with low RF, increased SAM, possibly released by the endothelial cells, might reflect the cytokine-induced activation of the vascular endothelium and the extravasation of some CD45RO+ T-PBL. PMID:7534432

Neidhart, M; Pataki, F; Fehr, K

1995-03-01

234

Intrauterine Adhesions  

MedlinePLUS

... causes of adhesion formation are infections of the uterine lining (endometritis), removal of fibroids in the cavity of the uterus and endometrial ablation (a surgical procedure that is used to intentionally damage the uterine lining to eliminate menstrual periods or make periods ...

235

Polyimide Adhesives.  

National Technical Information Service (NTIS)

A process of preparing aromatic polyamide-acids for use as adhesives is described. An equimolar quantity of an aromatic dianhydride is added to a stirred solution of an aromatic diamine in a water or alcohol-miscible ether solvent to obtain a viscous poly...

D. J. Progar V. L. Bell T. L. Saintclair

1974-01-01

236

ELAM1 Mediates Cell Adhesion by Recognition of a Carbohydrate Ligand, Sialyl-Le^x  

Microsoft Academic Search

Recruitment of neutrophils to sites of inflammation is mediated in part by endothelial leukocyte adhesion molecule-1 (ELAM-1), which is expressed on activated endothelial cells of the blood vessel walls. ELAM-1 is a member of the LEC-CAM or selectin family of adhesion molecules that contain a lectin motif thought to recognize carbohydrate ligands. In this report, cell adhesion by ELAM-1 is

M. Laurie Phillips; Edward Nudelman; Federico C. A. Gaeta; Mary Perez; Anil K. Singhal; Sen-Itiroh Hakomori; James C. Paulson

1990-01-01

237

Adhesive capsulitis.  

PubMed

Adhesive capsulitis of the shoulder, commonly known as "frozen shoulder" or "frozen shoulder syndrome," is a self-limited painful condition that is quite common. In 1984, the prevalence of frozen shoulder was demonstrated at slightly greater than 2% in the general population. In the authors' practice, consisting primarily of orthopedic magnetic resonance imaging, this diagnosis is frequently seen in patients referred for evaluation of rotator cuff tear because the presenting symptoms are similar. PMID:24875344

Pomeranz, Stephen J; Modi, Neeraj

2014-01-01

238

Polyimide adhesives  

NASA Technical Reports Server (NTRS)

A process was developed for preparing aromatic polyamide acids for use as adhesives by reacting an aromatic dianhydride to an approximately equimolar amount of an aromatic diamine in a water or lower alkanol miscible ether solvent. The polyamide acids are converted to polyimides by heating to the temperature range of 200 - 300 C. The polyimides are thermally stable and insoluble in ethers and other organic solvents.

Progar, D. J.; Bell, V. L.; Stclair, T. L. (inventors)

1977-01-01

239

Antibodies to Intercellular Adhesion Molecule 1\\/Lymphocyte Function-associated Antigen 1 Prevent Crescent Formation in Rat Autoimmune Glomerulonephritis  

Microsoft Academic Search

SBmlTlftry In patients with glomerulonephritis widespread crescents are associated with a poor prognosis. Crescent formation appears to depend on the migration of mononuclear cells into Bowman's space, and therefore the interaction between leukocytes and glomerular endothelium may be a critical event in the genesis of crescents. We performed the present study to determine the effects of mouse monoclonal antibodies to

Kazuhiro Nishikawa; Ya-Jun Guo; Masayuki Miyasaka; Takuya Tamatani; A. Bernard Collins; Man-Sun Sy; Robert T. McCluskey; Giuseppe Andres

240

Influence of cytokine and intercellular adhesion molecule-1 gene polymorphisms on acute rejection in pediatric renal transplantation.  

PubMed

Immune response regulation by cytokines is a key to understanding AGR. The influence of the functional polymorphisms in genes coding for TNF-alpha (-308G > A), IL-10 (-819C > T, and -1082A > G), IFN-gamma [(CA)n], TGF-beta1 (+869T > C), and iCAM-1 (R241G and E469K), in addition to HLA and gender matching on the presentation of AGR in 51 pediatric renal recipients during a 36-month post-transplantation follow-up were analyzed. Also, donors and a control group were genotyped. All groups were within Hardy-Weinberg equilibrium for all polymorphisms except IL-10-819C > T and TNF-alpha (p < 0.005 and p < 0.01, respectively) in recipients. Transplants with gender mismatch showed a higher risk for AGR than those between individuals with gender match (OR, 4.227; p = 0.010). Recipients with a high-production compared with low-production TNF-alpha allele experienced earlier AGR (p = 0.030), and those with high-production alleles of both TNF-alpha and IFN-gamma showed a further increased risk (OR = 11.129, p = 0.024). These findings support the notion that a single genotype cannot by itself explain an event as complex as AGR. The sum or combination of different specific alleles of these genes could better account for the immune response to an allograft. PMID:18627514

Mendoza-Carrera, Francisco; Ojeda-Durán, Simón; Angulo, Eduardo; Rivas, Fernando; Macías-López, Griselda; Buen, Eliseo Portilla-de; Leal, Caridad

2008-11-01

241

Diesel exhaust particles up-regulate expression of intercellular adhesion molecule-1 (ICAM-1) in human bronchial epithelial cells  

PubMed Central

Epidemiological and experimental studies suggest that diesel exhaust particles (DEP) may play an active role in the increased respiratory mortality and morbidity. We have shown that DEP augmented the production of inflammatory cytokines by human airway epithelial cells in vitro. ICAM-1 has been shown to play an important role in the local accumulation of inflammatory cells. We studied the effect of DEP on ICAM-1 gene expression and surface expression in human bronchial epithelial cell line BEAS-2B. DEP (5–50 ?g/ml) showed a stimulatory effect on ICAM-1 mRNA levels as evaluated by reverse transcription-polymerase chain reaction (RT-PCR). Flow cytometric analysis demonstrated an increased ICAM-1 expression on the epithelial cell surfaces. The soluble form of ICAM-1 molecules was also increased by the stimulation of DEP. In vitro neutrophil attachment onto DEP-stimulated epithelial cells was augmented, which was partially blocked by anti-ICAM-1 neutralizing antibody. Finally, these events were significantly inhibited by pretreatment with anti-oxidants pyrrolidine dithiocarbamate and N-acetyl cysteine, and p38 mitogen activated protein kinase (MAPK) inhibitor SB203580. These findings suggested that DEP induced up-regulation of ICAM-1 gene, and this process might be largely dependent on oxidant-mediated NF-?B activation and p38-MAPK pathways.

Takizawa, H; Abe, S; Ohtoshi, T; Kawasaki, S; Takami, K; Desaki, M; Sugawara, I; Hashimoto, S; Azuma, A; Nakahara, K; Kudoh, S

2000-01-01

242

Intercellular Adhesion Molecule1 is Expressed on Human Granulosa Cells and Mediates Their Binding to Lymphoid Cells  

Microsoft Academic Search

Some immune cellular components have been recently demon- strated to play a critical role in ovarian physiology. Resident ovarian white blood cells are known to produce cytokines that modulate gran- ulosa cell (GC) functions and differentiation. Moreover, it has been postulated that, during the formation of the corpus luteum and lu- teolysis, human luteal cells are able to interact with

PAOLA VIGANO; BARBARA GAFFURI; GUIDO RAGNI; ANNA MARIA DI BLASIO

2010-01-01

243

Talc-induced Expression of CC and C-X-C Chemokines and Intercellular Adhesion Molecule1 in Mesothelial Cells  

Microsoft Academic Search

Treatment of symptomatic carcinomatous pleural effusions is primarily directed at local palliation with a wide variety of sclerosing agents, of which talc is considered to be the most successful. The mechanism whereby talc achieves this effect is unknown. The objective of this study was to investi- gate whether talc stimulates pleural mesothelial cells (PMC) to release C-X-C and\\/or C-C chemokines

NAJMUNNISA NASREEN; DANIEL L. HARTMAN; KAMAL A. MOHAMMED; VEENA B. ANTONY

1998-01-01

244

Platelet endothelial cell adhesion molecule-1 serves as an inhibitory receptor that modulates platelet responses to collagen  

Microsoft Academic Search

nized member of the inhibitory receptor fam- ily, contains a functional immunoreceptor tyrosine-based inhibitory motif within its cy- toplasmic domain that, when tyrosine phos- phorylated, recruits and activates the pro- tein-tyrosine phosphatase, SHP-2. To test the hypothesis that PECAM-1 functions to regulate GPVI\\/FcRg-chain-mediated plate- let activation, the responses of wild-type versus PECAM-1-deficient murine platelets to GPVI-specific agonists were compared. Four

Sonali Patil; Debra K. Newman; Peter J. Newman

2001-01-01

245

Prediction of Veno-Occlusive Disease Using Biomarkers of Endothelial Injury  

PubMed Central

Predicting the development of veno-occlusive disease of the liver (VOD) remains challenging. We hypothesized that biomarkers of endothelial injury in myeloablative allogeneic transplant recipients could predict VOD occurrence. We evaluated 4 biomarkers (von Willebrand Factor (vWF), thrombomodulin, E-selectin and soluble intercellular adhesion molecule-1 (sICAM-1) weekly in the peri-transplant period in an attempt to predict VOD. Among patients who received sirolimus, vWF, thrombomodulin and sICAM-1 levels were significantly elevated in VOD patients in comparison with patients without VOD on day ?1 (p?0.035), day+7 (p?0.0001) and day+14 (p?0.004). E-selectin was predictive on day+7 (p=0.007). vWF ?1400 IU/ml and TM ? 100 ng/ml levels on day +7 were both 100% sensitive and 100% specific in predicting VOD. These biomarkers were informative when adjusted for other risk factors for VOD in regression analysis. Among non-sirolimus patients, biomarkers of endothelial injury were not informative. We conclude that vWF, thrombomodulin and sICAM-1 elevations before and early after transplantation may be useful in predicting VOD in patients receiving sirolimus.

Cutler, Corey; Kim, Haesook T.; Ayanian, Shake; Bradwin, Gary; Revta, Carolyn; Aldridge, Julie; Ho, Vincent; Alyea, Edwin; Koreth, John; Armand, Philippe; Soiffer, Robert; Ritz, Jerome; Richardson, Paul G.; Antin, Joseph H.

2010-01-01

246

Temperature Modulation of Integrin-Mediated Cell Adhesion  

PubMed Central

In response to external stimuli, cells modulate their adhesive state by regulating the number and intrinsic affinity of receptor/ligand bonds. A number of studies have shown that cell adhesion is dramatically reduced at room or lower temperatures as compared with physiological temperature. However, the underlying mechanism that modulates adhesion is still unclear. Here, we investigated the adhesion of the monocytic cell line THP-1 to a surface coated with intercellular adhesion molecule-1 (ICAM-1) as a function of temperature. THP-1 cells express the integrin lymphocyte function-associated antigen-1 (LFA-1), a receptor for ICAM-1. Direct force measurements of cell adhesion and cell elasticity were carried out by atomic force microscopy. Force measurements revealed an increase of the work of de-adhesion with temperature that was coupled to a gradual decrease in cellular stiffness. Of interest, single-molecule measurements revealed that the rupture force of the LFA-1/ICAM-1 complex decreased with temperature. A detailed analysis of the force curves indicated that temperature-modulated cell adhesion was mainly due to the enhanced ability of cells to deform and to form a greater number of longer membrane tethers at physiological temperatures. Together, these results emphasize the importance of cell mechanics and membrane-cytoskeleton interaction on the modulation of cell adhesion.

Rico, Felix; Chu, Calvin; Abdulreda, Midhat H.; Qin, Yujing; Moy, Vincent T.

2010-01-01

247

Inability of plasma high-density lipoproteins to inhibit cell adhesion molecule expression in human coronary artery endothelial cells  

Microsoft Academic Search

High-density lipoproteins (HDL) have several antiatherogenic actions, including the ability to sequester cellular cholesterol, to protect low-density lipoproteins from oxidation and to inhibit platelet aggregation. An early event in atherogenesis is the adhesion and recruitment of blood monocytes, a process mediated by cell adhesion molecules (CAMs), including vascular cell adhesion molecule-1 (VCAM-1) which is rapidly synthesized by endothelial cells in

Anita K. Stannard; Shabeena Khan; Annette Graham; James S. Owen; Sean P. Allen

2001-01-01

248

Immunological and clinical follow up of hepatitis C virus associated cryoglobulinaemic vasculitis  

PubMed Central

OBJECTIVE—To study immunological markers and compare these markers with standard measures for the clinical and immunological follow up of vasculitis activity in hepatitis C virus (HCV) associated cryoglobulinaemic vasculitis (CV).?METHODS—Serial serum samples from eight patients with newly diagnosed HCV associated CV were followed during interferon ? treatment induced remission of the CV. Vasculitis activity and disease extent were evaluated with the Birmingham vasculitis activity score (BVAS) and disease extent index (DEI). Cryoglobulinaemia, complement levels (C3c, C4, and CH50), rheumatoid factor (RF), autoantibodies such as antinuclear antibodies, soluble interleukin 2 receptor (sIL2r), soluble intercellular adhesion molecule-1 (sICAM-1), and soluble CD30 (sCD30) were determined.?RESULTS—All patients achieved either complete or partial remission of their CV during interferon ? treatment. There was a significant reduction in vasculitis activity and disease extent (BVAS, DEI), cryoglobulinaemia, RF, sIL2r, sICAM-1, and sCD30. Complement C3c levels increased significantly during this period. Erythrocyte sedimentation rate and levels of complement C4 and CH50 did not change significantly. Both clinical measures (BVAS and DEI) correlated significantly only with C3c and sCD30.?CONCLUSIONS—Although this study was of only a small group of patients, it shows that BVAS and DEI as clinical measures and C3c and sCD30 as immunological markers may be useful in the follow up of disease activity of HCV associated CV. The data indicate that activity of the humoral (cryoglobulinaemia, RF, autoantibodies) and cellular (sIL2r, sICAM-1, sCD30) immune response and endothelial damage (sICAM-1) are found in HCV associated CV.??

Lamprecht, P; Moosig, F; Gause, A; Herlyn, K; Csernok, E; Hansen, H; Gross, W

2001-01-01

249

Periatrial Epicardial Fat Is Associated with Markers of Endothelial Dysfunction in Patients with Atrial Fibrillation  

PubMed Central

Background Epicardial adipose tissue (EAT) is associated to atrial fibrillation (AF) burden and outcome after AF ablation. We intended to determine whether global or local EAT is associated with systemic and/or left atrial (LA) inflammation and markers of endothelial dysfunction in AF patients. Methods and Results Total, atrial, and ventricular EAT volume (EATtotal, EATatrial, EATventricular) were measured by multislice cardiac CT in 49 patients with paroxysmal (PAF, n=25) or persistent AF (PeF, n=24). Periatrial epicardial fat thickness at the esophagus (LA-ESO) and thoracic aorta (LA-ThA) were also measured. Vascular endothelial growth factor (VEGF), interleukin-8 (IL-8), soluble intercellular adhesion molecule 1 (sICAM-1), transforming growth factor-?1 (TGF-?1), and von Willebrand Factor (vWF) levels were measured in peripheral and LA blood samples obtained during catheterization during AF ablation. Patients with PeF had higher EATatrial (P<0.05) and LA-ESO (P=0.04) than patients with PAF. VEGF, IL-8, and TGF-?1 were not associated with EAT. In contrast, after adjusting for LA volume and body mass index, higher LA-ThA was significantly associated with higher sICAM-1 and vWF levels, both in peripheral blood (P<0.05) and in LA (P<0.05). Similar results were found with LA-ESO. Body mass index, EATtotal and EATventricular were not associated with sICAM-1 and vWF. Conclusions Periatrial epicardial fat showed a significant positive association with increased levels of sICAM-1 and vWF, which are biomarkers of endothelial dysfunction. No such associations were found when considering body mass index or EATtotal. These results suggest that local EAT rather than regional or total adiposity may modulate endothelial dysfunction in patients with AF.

Girerd, Nicolas; Scridon, Alina; Bessiere, Francis; Chauveau, Samuel; Geloen, Alain; Boussel, Loic; Morel, Elodie; Chevalier, Philippe

2013-01-01

250

Understanding Marine Mussel Adhesion  

PubMed Central

In addition to identifying the proteins that have a role in underwater adhesion by marine mussels, research efforts have focused on identifying the genes responsible for the adhesive proteins, environmental factors that may influence protein production, and strategies for producing natural adhesives similar to the native mussel adhesive proteins. The production-scale availability of recombinant mussel adhesive proteins will enable researchers to formulate adhesives that are water-impervious and ecologically safe and can bind materials ranging from glass, plastics, metals, and wood to materials, such as bone or teeth, biological organisms, and other chemicals or molecules. Unfortunately, as of yet scientists have been unable to duplicate the processes that marine mussels use to create adhesive structures. This study provides a background on adhesive proteins identified in the blue mussel, Mytilus edulis, and introduces our research interests and discusses the future for continued research related to mussel adhesion.

Roberto, Francisco F.

2007-01-01

251

Understanding Marine Mussel Adhesion  

SciTech Connect

In addition to identifying the proteins that have a role in underwater adhesion by marine mussels, research efforts have focused on identifying the genes responsible for the adhesive proteins, environmental factors that may influence protein production, and strategies for producing natural adhesives similar to the native mussel adhesive proteins. The production-scale availability of recombinant mussel adhesive proteins will enable researchers to formulate adhesives that are waterimpervious and ecologically safe and can bind materials ranging from glass, plastics, metals, and wood to materials, such as bone or teeth, biological organisms, and other chemicals or molecules. Unfortunately, as of yet scientists have been unable to duplicate the processes that marine mussels use to create adhesive structures. This study provides a background on adhesive proteins identified in the blue mussel, Mytilus edulis, and introduces our research interests and discusses the future for continued research related to mussel adhesion.

H. G. Silverman; F. F. Roberto

2007-12-01

252

Kidney injury molecule-1 outperforms traditional biomarkers of kidney injury in preclinical biomarker qualification studies  

Microsoft Academic Search

Kidney toxicity accounts both for the failure of many drug candidates as well as considerable patient morbidity. Whereas histopathology remains the gold standard for nephrotoxicity in animal systems, serum creatinine (SCr) and blood urea nitrogen (BUN) are the primary options for monitoring kidney dysfunction in humans. The transmembrane tubular protein kidney injury molecule-1 (Kim-1) was previously reported to be markedly

Frank Dieterle; Fitz B Collings; Victoria Ramirez; Sean Troth; Nagaraja Muniappa; Douglas Thudium; David Gerhold; Daniel J Holder; Norma A Bobadilla; Estelle Marrer; Elias Perentes; André Cordier; Jacky Vonderscher; Gérard Maurer; Peter L Goering; Joseph V Bonventre; Vishal S Vaidya; Josef S Ozer; Frank D Sistare

2010-01-01

253

Analysis of adhesion molecules in Ki1 anaplastic large-cell lymphoma  

Microsoft Academic Search

We analysed the expression of adhesion molecules on lymphoma cells in 13 patients with Ki-1 (CD30)-positive anaplastic large-cell lymphoma (Ki-1 ALCL; lymph nodes in 6, extranodal tumours in 6, and both lymph nodes and bone in 1). Very late activation antigen (VLA)-a4 (CD49d) and Hermes lymph node homing receptor (CD44) were constantly expressed in all specimens, and intercellular adhesion molecule-1

M. Akamatsu; M. Takeshita; K. Ohshima; M. Kikuchi; J. Suzumiya

1994-01-01

254

ICAM-1 expression by lung cancer cell lines: effects of upregulation by cytokines on the interaction with LAK cells.  

PubMed

Intercellular adhesion molecule-1 (ICAM-1) expression by tumour cells may be involved in their interaction with defensive cells. In this study the surface ICAM-1 expression and soluble ICAM-1 (sICAM-1) production by five small cell lung cancer (SCLC) and five non-SCLC (NSCLC) cell lines was investigated. In addition, the effects of ICAM-1 upregulation by cytokines on the adhesion of lung cancer cells to allogeneic lymphokine-activated killer (LAK) cells and susceptibility to LAK cytotoxicity was also evaluated. ICAM-1 expression was assessed by flow cytometry. Soluble ICAM-1 release was measured by enzyme-linked immunosorbent assay (ELISA). Interaction with LAK cells was tested by adhesion and cytotoxicity assays. At baseline, SCLC lines did not express ICAM-1, while 4 of the 5 NSCLC lines expressed ICAM-1. ICAM-1 expression was induced by interferon-gamma (IFN-gamma) in 4 of the 5 SCLC lines and upregulated in 1 of the 5 NSCLC lines. ICAM-1 expression was induced by tumour necrosis factor-alpha (TNF-alpha) in 1 of the 5 SCLC lines (National Cancer Institute (NCI) H211), and upregulated in 2 of the 5 NSCLC lines (NCI H460 and NCI H838). Among the latter lines, one (NCI H838) released significant amounts of sICAM-1. Adhesion to LAK cells and susceptibility to LAK cytotoxicity were significantly higher in TNF-alpha-treated NCI H460 and NCI H211 cells, compared to untreated NCI H460 and NCI H211 cells. In contrast, no difference in adhesion to LAK cells and susceptibility to LAK cytotoxicity was detected between baseline and TNF-alpha-treated NCI H838 cells. Intercellular adhesion molecule-1 surface expression and soluble intercellular adhesion molecule-1 release may play an important role in interactions between lymphokine-activated killer cells and lung cancer cells. PMID:8880099

Melis, M; Spatafora, M; Melodia, A; Pace, E; Gjomarkaj, M; Merendino, A M; Bonsignore, G

1996-09-01

255

Adhesive and conductive adhesive flip chip bonding  

Microsoft Academic Search

Over the past decade the use of adhesives for electronic interconnect has been driven by the explosive growth of flat panel liquid crystal displays (LCD). Developed and used primarily by Japanese manufacturers of consumer products, particle-loaded adhesive films fulfilled a need in LCDs that could not be met by solder reflow: low temperature, high line density (to 50 ?m pitch)

R. L. D. Zenner; G. Connell; J. A. Gerber

1997-01-01

256

Beam Test for Adhesives.  

National Technical Information Service (NTIS)

The strength of materials solution for a new bonded cantilever beam test specimen to determine adhesive shear properties is reviewed and discussed. A parametric analysis for the adhesive shear stress and for the end deflection reveals the specimen dimensi...

V. F. Fior H. F. Brinson

1988-01-01

257

Maternal Biomarkers of Endothelial Dysfunction and Preterm Delivery  

PubMed Central

Background Endothelial dysfunction is key to the development of atherosclerosis. Preterm delivery foreshadows later maternal cardiovascular disease (CVD), but it is not known if endothelial dysfunction also occurs. We prospectively measured circulating biomarkers of endothelial dysfunction in pregnant women with preterm or term delivery. Methods We conducted a case-control study nested within a large prospective epidemiological study of young, generally healthy pregnant women. Women who delivered preterm (<37 completed weeks gestation, n?=?240) and controls who delivered at term (n?=?439) were included. Pregnancies complicated by preeclampsia were analyzed separately. Circulating endothelial dysfunction biomarkers included soluble intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (sVCAM-1) and soluble E-selectin (sE-selectin). Results Elevated levels of sICAM-1 and sVCAM-1 were positively associated with preterm delivery independent of usual risk factors. At entry (?16 wks), the adjusted odds ratio (AOR) was 1.73 (95% confidence interval (CI) 1.09–2.74) for the highest quartile of sICAM-1 versus the lowest quartile and for sVCAM-1 the AOR was 2.17 (95% CI 1.36–3.46). When analysis was limited to cases with a spontaneous preterm delivery, the results were unchanged. Similar results were obtained for the 3rd trimester (?30 wks). Elevated sE-selectin was increased only in preterm delivery complicated by preeclampsia; risk was increased at entry (AOR 2.32, 95% CI 1.22–4.40) and in the 3rd trimester (AOR 3.37, 95% CI 1.78–6.39). Conclusions Impaired endothelial function as indicated by increased levels of soluble molecules commonly secreted by endothelial cells is a pathogenic precursor to CVD that is also present in women with preterm delivery. Our findings underscore the need for follow-up studies to determine if improving endothelial function prevents later CVD risk in women.

Chen, Xinhua; Scholl, Theresa O.

2014-01-01

258

Adhesion Prevention in Myomectomy  

PubMed Central

Adhesions are abnormal fibrous connections, joining tissue surfaces in abnormal locations. Adhesions form after any trauma involving the peritoneum and the injured tissue surface or directly between the injured tissue surfaces. The ideal anti-adhesion agent should be safe, efficacious, easy to use in all types of surgery, and economical. It should prevent adhesions at the site of surgery as well as throughout the peritoneal cavity. Needless to say, the ideal agent is still elusive.

Pal, Bhaskar

2011-01-01

259

Adhesive gravitational clustering  

Microsoft Academic Search

The notion of adhesion has been advanced for the phenomenon of stabilization of large-scale structure emerging from gravitational instability of a cold medium. Recently, the physical origin of adhesion has been identified: a systematic derivation of the equations of motion for the density and the velocity fields leads naturally to the key equation of the ``adhesion approximation'' - however, under

Thomas Buchert; A. Domínguez

2005-01-01

260

Pentoxifylline Decreases Serum Level of Adhesion Molecules in Atherosclerosis Patients  

PubMed Central

Background: Inflammation is involved in development, progression, and complications of atherosclerotic disease. Clinical studies have indicated that the level of monocyte chemoattractant protein 1 (MCP-1), IL-18, and adhesion molecules correlates with the severity of atherosclerosis and can predict future cardiovascular events. Experimental studies have shown pentoxifylline (PTX) reduces these factors in animal models. The purpose of the present pilot study was to evaluate effect of PTX on a group of inflammatory biomarkers in patients with coronary artery disease (CAD). Methods: Forty patients with angiographically documented CAD, who fulfilled inclusion and exclusion criteria, were entered in the double-blind, randomized, pilot clinical study. The patients were randomly given PTX (400 mg three times daily) or placebo (3 tab/day) for 2 months. Serum concentrations of MCP-1, IL-18, intercellular adhesion Molecule 1 (ICAM-1), and vascular cell adhesion molecule 1 (VCAM-1) were measured before and at the end of intervention by enzyme-linked immunosorbant assay. Results: Our study showed that the serum levels of ICAM-1 and VCAM-1 was decreased in the study population after two-month treatment (P<0.05). Conclusion: Based on the results of our pilot study, administration of PTX in CAD patients significantly decreases adhesion molecules levels.

Mohammadpour, Amir Hooshang; Falsoleiman, Homa; Shamsara, Jamal; Abadi, Ghazaleh Allah; Rasooli, Ramin; Ramezani, Mohammad

2014-01-01

261

White blood cell deformation and firm adhesion  

NASA Astrophysics Data System (ADS)

For a white blood cell (WBC) to arrive at infection sites, it forms chemical attachments with activated endothelial cells. First, it bonds with P-selectin, which holds it to the wall, but weakly; this allows the WBC to roll under the shear flow of the blood around it. Later, the WBCs bond with the stronger intracellular adhesion molecule-1 (ICAM-1); it is these ICAM bonds that allow the WBCs to fully resist the flow and stop rolling, allowing them to crawl through the endothelial wall. We model this numerically. Our model uses the immersed boundary method to represent the interaction of the shear flow with the deformable cell membrane. Receptors are on the tips of microvilli-little fingers sticking off of the cell membrane. The microvilli also deform. The receptors stochastically form and break bonds with molecules on the wall. Using this method, the history of each microvillus and its bonds can be found, as well as the distribution of the adhesion traction forces and how all of these vary with the deformability of the white blood cell. At higher shear rates, the white blood cell membrane deforms more, increasing its contact area with the surface; this effect is larger for softer membranes. We investigate how the deformability of the WBC affects the ease with which it forms firm adhesion.

Szatmary, Alex; Eggleton, Charles

2011-11-01

262

Rolling cell adhesion  

PubMed Central

Rolling adhesion on vascular surfaces is the first step in recruiting circulating leukocytes, hematopoietic progenitors, or platelets to specific organs or to sites of infection or injury. Rolling requires the rapid yet balanced formation and dissociation of adhesive bonds in the challenging environment of blood flow. This review explores how structurally distinct adhesion receptors interact through mechanically regulated kinetics with their ligands to meet these challenges. Remarkably, increasing force applied to adhesive bonds first prolongs their lifetimes (catch bonds) and then shortens their lifetimes (slip bonds). Catch bonds mediate the counterintuitive phenomenon of flow-enhanced rolling adhesion. Force-regulated disruptions of receptor interdomain or intradomain interactions remote from the ligand-binding surface generate catch bonds. Adhesion receptor dimerization, clustering in membrane domains, and interactions with the cytoskeleton modulate the forces applied to bonds. Both inside-out and outside-in cell signals regulate these processes.

McEver, Rodger P.; Zhu, Cheng

2013-01-01

263

Continuous heparinization and circulating adhesion molecules in the critically ill.  

PubMed

Endothelial activation and damage are common endpoints of a complex process that may result in multiple organ dysfunction syndrome (MODS). The influence of continuous intravenous heparinization on plasma levels of circulating adhesion molecules was studied in 28 trauma patients (injury severity score between 15 and 25 points) and 28 sepsis patients secondary to abdominal surgery. According to a prospective, randomized sequence the patients received either unfractionated heparin (aim: activated partial thromboplastin time (aPTT) approximately 2 x normal) (trauma-heparin (n = 14); sepsis-heparin (n = 14)) or not (trauma (n = 14); sepsis (n = 14)). Plasma levels of circulating soluble endothelial leukocyte adhesion molecule-1 (sELAM-1), vascular cell adhesion molecule-1 (sVCAM-1), intercellular adhesion molecule-1 (slCAM-1), and granule membrane protein-140 (sGMP-140) were serially measured from arterial blood samples for 5 days. Approximately 600 U/h of heparin were given to increase aPTT to approximately 60 s. Plasma levels of all adhesion molecules increased in all groups. This increase was significantly (p < .05) highest in both sepsis groups (sepsis: sELAM-1: from 50+/-11 to 84+/-19 ng/mL; slCAM-1: 410+/-68 to 700+/-95 ng/mL), but did not differ significantly between the treated and nontreated patients (sepsis-heparin: sELAM-1: from 60+/-131 to 88+/-20 ng/mL; slCAM-1: from 398+/-99 to 686+/-119 ng/mL). Trauma patients showed a less pronounced increase in all adhesion molecules without differences between the two subgroups. Only sGMP-140 increased significantly (p < .05) more in the trauma (from 102+/-20 to 169+/-16 ng/mL) than in the trauma-heparin group (from 109+/-19 to 132+/-17 ng/mL). It is summarized that continuous heparinization with approximately 600 U/h did not attenuate the rise in circulating adhesion molecules in sepsis and trauma patients. The study findings suggest that heparin in this dose regimen may be unlikely to influence endothelial inflammation or endothelial function in critically ill patients. PMID:9921711

Boldt, J; Papsdorf, M; Piper, S N; Rothe, A; Hempelmann, G

1999-01-01

264

Activated Endothelium Binds Lymphocytes Through a Novel Binding Site in the Alternately Spliced Domain of Vascular Cell Adhesion Molecuh-1  

Microsoft Academic Search

Summary Vascular cell adhesion molecule-1 (VCAM-1) is induced on endothdial cells by inflammatory cytokines, and binds mononuclear leukocytes through the integrin very late antigen-4 (VLA-4) (o14B1). This adhesion pathway has been implicated in a diverse group of physiological and pathological processes, including B cell development, leukocyte activation and recruitment to sites of inflammation, atherosderosis, and tumor cell metastasis. The major

Laurelee Osborn; Cornelia Vassallo; Christopher D. Benjamin

265

Obesity modifies the association between plasma phospholipid polyunsaturated fatty acids and markers of inflammation: the Multi-Ethnic Study of Atherosclerosis  

PubMed Central

Background and objective Systemic inflammation is a well-known risk factor for diseases such as atherosclerosis and is augmented by the presence of obesity. In addition, it has been shown that inflammation may be negatively influenced by certain macronutrients, specifically the omega-3 and omega-6 fatty acids. The primary aim of this study is to determine whether obesity modifies the association between plasma phospholipid polyunsaturated fatty acids (PUFAs) and markers of inflammation and endothelial activation in Multi-Ethnic Study of Atherosclerosis (MESA) participants. Subjects A sample of 2848 adults (25% African American, Chinese, Hispanic, and White) randomly selected from the MESA cohort. Measurements Relative plasma PUFA concentrations were determined using gas chromatography-flame ionization detection. Levels of three inflammatory markers (high-sensitivity C-reactive protein, interleukin (IL)-6 and tumor necrosis factor-receptor 1) and two endothelial activation markers (soluble intercellular adhesion molecule-1 (sICAM-1) and E-selectin) were determined with enzyme immunoassays. Linear regression analysis was used to evaluate the relationship between these markers and plasma PUFAs. Results Obesity modified the associations of linoleic acid (Pint=0.01), dihomo-?-linolenic (Pint=0.07) and eicosapentaenoic acid (EPA) (Pint=0.04) with sICAM-1 concentrations; in addition, obesity modified the association of IL-6 with dihomo-?-linolenic (Pint=0.01). In obese individuals, sICAM-1 was inversely related to EPA levels (P=0.02), but directly related to linoleic acid levels (P<0.001). Conversely, sICAM-1 was inversely related to linoleic acid levels in normal weight individuals (P=0.04). IL-6 concentrations were significantly and directly related to dihomo-?-linolenic acid (DGLA) in normal weight (P=0.01) and obese participants (P<0.001), but the scale of increase across tertiles was greater in obese adults. Main effects of fatty acid and inflammatory marker associations are also reported. Conclusion The modifying effect of obesity on the association of plasma PUFAs with IL-6 and sICAM-1 suggests differences in fatty acid metabolism and may also have implications in dietary fatty acid intake for obese individuals, particularly for linoleic and EPAs. Further study is warranted to confirm and explain the strong associations of DGLA with inflammatory and endothelial activation markers.

Steffen, BT; Steffen, LM; Tracy, R; Siscovick, D; Hanson, NQ; Nettleton, J; Tsai, MY

2014-01-01

266

Role of inflammation in previously untreated macular edema with branch retinal vein occlusion  

PubMed Central

Background The association of inflammatory factors and the aqueous flare value with macular edema in branch retinal vein occlusion (BRVO) patients remains unclear. The relationship between the aqueous flare value and the vitreous fluid levels of vascular endothelial growth factor (VEGF), interleukin (IL)-6, monocyte chemotactic protein (MCP)-1, soluble intercellular adhesion molecule 1 (sICAM-1), and soluble VEGF receptor-2 (sVEGFR-2) was evaluated to investigate the role of inflammation in BRVO associated with macular edema. Aqueous flare values and the vitreous levels of VEGF, IL-6, MCP-1, sICAM-1, and sVEGFR-2 were compared between previously untreated patients with BRVO and patients with macular hole (MH). Methods Vitreous samples were obtained from 45 patients during vitreoretinal surgery (28 patients with BRVO and 17 with MH), and the levels of VEGF, IL-6, MCP-1, sICAM-1, and sVEGFR-2 were measured by enzyme-linked immunosorbent assay. Retinal ischemia was evaluated by measuring the area of capillary non-perfusion using fluorescein angiography and the Scion Image program. Aqueous flare values were measured with a laser flare meter and macular edema was examined by optical coherence tomography. Results The median aqueous flare value was significantly higher in the BRVO group (12.1 photon counts/ms) than in the MH group (4.5 photon counts/ms, P?

2014-01-01

267

Berberine hydrochloride prevents postsurgery intestinal adhesion and inflammation in rats.  

PubMed

Intestinal adhesion, characterized by connection of the loops of the intestine with other abdominal organs by fibrous tissue bands, remains an inevitable event of abdominal operations and can cause a number of complications. Berberine hydrochloride (berberine), a natural plant alkaloid derived from Chinese herbal medicine, is characterized by diverse pharmacological effects, such as anticancer and lower elevated blood glucose. This study is designed to investigate the effects of berberine on adhesion and inflammation after abdominal surgeries and the underlying molecular mechanisms. Adhesion severity grades and collagen deposition were assessed 14 days after surgery. We evaluated the levels of intercellular adhesion molecule-1 (ICAM-1) and inflammatory cytokines interleukin-1? (IL-1?), IL-6, transforming growth factor ? (TGF-?), tumor necrosis factor-? (TNF-?), and examined transforming growth factor-activated kinase 1 (TAK1)/c-Jun N-terminal kinase (JNK) and TAK1/nuclear factor ?B (NF-?B) signaling. The surgery group experienced the most severe adhesions, and berberine strikingly reduced the density and severity of adhesion. Results showed significant lower expression of IL-1?, IL-6, TGF-?, TNF-?, and ICAM-1, in berberine groups compared with the operation group. Activities of phosphorylated JNK and phosphorylated NF-?B were inhibited in the berberine groups compared with the surgery group. Our novel findings identified berberine hydrochloride as a promising strategy to prevent adhesion by downregulating ICAM-1 and reduce inflammation by inhibiting the TAK1/JNK and TAK1/NF-?B signaling after abdominal surgery, which brought out a good therapeutic approach for the development of clinical application for postoperative abdominal adhesion and inflammation. PMID:24676878

Zhang, Yong; Li, Xiaoguang; Zhang, Qingwei; Li, Jiamin; Ju, Jiaming; Du, Ning; Liu, Xin; Chen, Xiaohui; Cheng, Feiran; Yang, Lei; Xu, Chaoqian; Bilal, Muhammad U; Wei, Yunwei; Lu, Yanjie; Yang, Baofeng

2014-06-01

268

Methods for Treating Adhesive Capsulitis.  

National Technical Information Service (NTIS)

The invention relates to the discovery that collagenase injections are effective in lyse the collagenous adhesions in the shoulder and treat the disorder, adhesive capsulitis. As such, the invention relates to methods of treating or preventing adhesive ca...

M. A. Badalamente

2006-01-01

269

Adhesive Guard Hair Removal.  

National Technical Information Service (NTIS)

Long hairs of fur pelts known as guard hairs are removed to reveal soft underfur by contacting the pelt with a substrate coated with adhesive and then pulling the substrate away from the pelt. Recoverable or nonrecoverable adhesive systems may be used.

H. E. Hull

1976-01-01

270

Adhesive for composite bonding  

SciTech Connect

Adhesive bonding is a viable option for structural joining of carbon fiber reinforced epoxy composites. Recent examples from laboratory programs include a composite tube joined to a flared composite collar (skirt) to provide a means for mechanical attachment. Another application involves adhesive bonding of a close-tolerance composite ring to the inside of a tapered, cylindrical composite penetrator case in order to provide a load bearing surface for prestressing the internal package. The adhesive bond in both of these applications is the critical load bearing component and must sustain large shearing stresses in order to maintain the structural integrity and viability of the part. The ideal adhesive would be a low viscosity (<10 poise) liquid with a long pot life, good wetting characteristics and high ultimate shear strength when cured at moderate (<50{degree}C) temperature. An adhesive with these characteristics would allow for the production of defect-free bonds by capillary wetting or squeezing flow of the adhesive into the narrow (.005{double prime}) annular space between the concentric composite parts. Since adhesives possessing these characteristics were not known to be available commercially, candidate materials were evaluated for this application. In this paper we present bond shear strength data and selected physical properties for some epoxy adhesive formulations. 7 refs., 5 figs., 2 tabs.

Lyon, R.E.; Walkup, C.M.; Matthews, J.T.

1989-11-27

271

Physics of cell adhesion  

Microsoft Academic Search

Cell adhesive phenomena are important biological processes. They involve many different steps and a variety of intermolecular forces; hence quantitative considerations may prove necessary to understand them. Three points must be discussed before elaborating a theory of cell adhesion.Modelling of an ``average cell'' as a physical object. The cell surface may be viewed as a dense structure made of proteins

P. Bongrand; C. Capo; R. Depieds

1982-01-01

272

Dieneurethane adhesives in electronics  

Microsoft Academic Search

Gluing of electronic components in addition to soldering increase the reliability of electronic appliances used under vibration, thermal shocks and high humidity. Adhesives for this purpose should bond a variety of substrates and provide compatibility with electronic components. In this case, compatibility is a complex characteristic which excludes: corrosive effects on metal surfaces, especially on electronic components; absorption of adhesive

O. Figovsky; L. Sklyarsky

1998-01-01

273

Adhesives Mixer Applicator  

NASA Technical Reports Server (NTRS)

Two-part adhesives are stored, mixed, and dispensed by an applicator originally developed for use aboard the Space Shuttle orbiter. Compressed gas furnishes energy for mixing and dispensing. An operator needs only to open pressure valve and pull a trigger on dispenser nozzle to apply adhesive.

Ramos, D. O.; Werner, K. E.

1982-01-01

274

Neuron adhesion and strengthening  

NASA Astrophysics Data System (ADS)

Understanding the neuron/material adhesion is important for neuron stimulation and growth. The current challenges remain in the lack of precision of measuring techniques and understanding the behavior of neuron. Here, we report a fluid shear method to investigate adhesion at the neuron/poly-D-lysine interface. In this study, the adhesion of 12-day-old chick embryo-retina neurons cultured on poly-D-lysine coated glass coverslips was measured via parallel disk rotational flow. The shear stress experienced by the cells increases with the disk radius. There is a critical point along the radius (Rc) where the stress experienced by the neurons equals their adhesion. The measured Rc can be used to calculate the neuron adhesion. Our results demonstrate that neurons adhered to the poly-D-lysine had a strain hardening effect. The adhesive shear stress of the neuron-material increased with applied shear (?a). When the ?a reached or exceeded the value of 40 dyn/cm2, the adhesion remained constant at approximately 30 dyn/cm2. The present work allowed us not only to quantify the adhesive strength and force but also to evaluate the value of strain hardening at the neuron/poly-D-lysine interface.

Rocha, Aracely; Jian, Kuihuan; Ko, Gladys; Liang, Hong

2010-07-01

275

Organosilanes as adhesion promoters  

Microsoft Academic Search

The use of organosilanes as adhesion promoters for surface coatings, adhesives and syntactic foams is described and reviewed in the light of published work. Data are presented on the beneficial effect of silanes, when used as pretreatment primers and additives, on the bond strength of two pack epoxide and polyurethane paints applied to aluminium and mild steel. It is shown

P. Walker

1991-01-01

276

Diclofenac inhibits endothelial cell adhesion molecule expression induced with lipopolysaccharide.  

PubMed

Stimulation of cultured human umbilical vein endothelial cells (HUVEC) with lipopolysaccharide (LPS) induces adherence for human promyelocytic cell line HL60. Adherence of HL60 cells to HUVEC stimulated with LPS for 4 hr and for 24 hr were completely inhibited by pretreatment with diclofenac. While some other nonsteroidal antiinflammatory drugs (NSAIDs), such as ketoprofen, phenylbutazone, indomethacin, ibuprofen and acetylsaticylic acid, did not inhibit. The mechanism whereby diclofenac inhibits the adhesiveness of HUVEC was investigated. Pretreatment of diclofenac inhibited LPS-induced expression of E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in HUVEC, determined by flow cytometry and a cellular enzyme-linked immunosorbent assay (cell-ELISA). The inhibitory activity was concentration dependent between 15.6 and 250 micrograms/ml. Diclofenac also inhibited LPS-induced increases in E-selectin, ICAM-1 and VCAM-1 mRNAs, indicating that the action of diclofenac is to inhibit synthesis of these molecules. These data demonstrate that diclofenac is capable of inhibiting the expression of E-selectin, ICAM-1 and VCAM-1 in HUVEC. PMID:8691982

Sakai, A

1996-05-24

277

Traditional herbal remedies that influence cell adhesion molecule activity.  

PubMed

Many traditional medicines have demonstrated immune activity, however, research has largely neglected their effects on cell adhesion molecules (CAMs). This review reports on extracts from 37 medicinal plant species, similar to or replicating traditional preparations, that up- or downregulate either gene or protein activity of CAMs. The majority of the investigations were in vitro, primarily of the immunoglobulin superfamily of CAMs, specifically intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) and secondarily on the integrin (CD11b or MAC-1) and selectin (E-selectin and P-selectin) families of CAMs. The following plant species have demonstrated modulation of multiple CAMs: Artemisia asiatica, Boswellia serrata, Canscora decussata, Cinnamomum povectum, Dehaasia incrassate, Ganoderma lucidum, Ginkgo biloba, Hypericum perforatum, Juglans regia, Lycopus lucidus, Panax notoginseng, Rheum undulatum, Salvia miltiorrhiza. Many other species have documented activity on one CAM. Currently there are limited in vivo/ex vivo investigations, including a clinical trial on Mahonia aquifolium. Although further evidence is needed, the data suggest that the reviewed botanical medicines may have the potential to provide therapeutic potential in disease processes involving CAMs. Additionally, the reported success of many of these plant extracts by traditional cultures and modern phytotherapists may involve the modulation of CAMs. PMID:21105177

Spelman, K; Aldag, R; Hamman, A; Kwasnik, E M; Mahendra, M A; Obasi, T M; Morse, J; Williams, E J

2011-04-01

278

Cryogenic vacuum tight adhesive  

NASA Astrophysics Data System (ADS)

A synthetic adhesive for vacuum tight joints at cryogenic temperatures has been developed. It consists of three components, the main component being epoxy silicone organic resin. The joints made with the adhesive remain vacuum tight at liquid helium temperature, including superfluid helium. It was found possible to connect different materials with the adhesive (copper and stainless steel with each other, aluminum, aluminum alloys, fiberglass, etc.). The joints withstood thermal shock tests of ten repeated sharps cooling to liquid nitrogen temperature and heating in hot water. Using the adhesive a lot of different vacuum tight low temperature joints have been made. More than fifteen years of wide application of this adhesive in vacuum tight cryogenic joints proved its high reliability. Some designs of vacuum tight cryogenic joints are presented and the technique of their manufacturing is described.

Anashkin, O. P.; Keilin, V. E.; Patrikeev, V. M.

1999-12-01

279

Tissue adhesives in otorhinolaryngology  

PubMed Central

The development of medical tissue adhesives has a long history without finding an all-purpose tissue adhesive for clinical daily routine. This is caused by the specific demands which are made on a tissue adhesive, and the different areas of application. In otorhinolaryngology, on the one hand, this is the mucosal environment as well as the application on bones, cartilage and periphery nerves. On the other hand, there are stressed regions (skin, oral cavity, pharynx, oesophagus, trachea) and unstressed regions (middle ear, nose and paranasal sinuses, cranial bones). But due to the facts that adhesives can have considerable advantages in assuring surgery results, prevention of complications and so reduction of medical costs/treatment expenses, the search for new adhesives for use in otorhinolaryngology will be continued intensively. In parallel, appropriate application systems have to be developed for microscopic and endoscopic use.

Schneider, Gerlind

2011-01-01

280

Soluble interleukin-2 receptor is a thyroid hormone-dependent early-response marker in the treatment of thyrotoxicosis.  

PubMed Central

Thyrotoxic patients exhibit increased levels of immune activation molecules (soluble interleukin-2 receptor [sIL-2R], intercellular adhesion molecule-1 [ICAM-1], and endothelial-leukocyte adhesion molecule-1 [ELAM-1]) in serum, although the clinical significance of these measurements remains unclear. In a randomized 4-week study, we have recently shown that in the treatment of hyperthyroidism, the combination of cholestyramine and methimazole (MMI) resulted in faster lowering of serum thyroid-hormone levels than did MMI alone. Stored serial serum samples from patients participating in this randomized treatment trial were analyzed for sIL-2R, soluble ICAM-1 (sICAM-1), and soluble ELAM-1 (sELAM-1). The levels of all three molecules were elevated in patients with hyperthyroidism. Although the levels of sICAM-1 and sELAM-1 remained elevated through the 4-week follow-up period in both groups of patients, the sIL-2R levels (normal levels, 1.0 to 4.2 ng/ml) decreased significantly in the 10 patients who received cholestyramine in addition to MMI (week 0, 14.2 +/- 1.5 ng/ml; week 2, 10.8 +/- 1.2 ng/ml; week 4, 8.9 +/- 1.5 ng/ml). In eight patients who received MMI alone, sIL-2R decreased less rapidly (week 0, 12.3 +/- 1.4 ng/ml; week 2, 12.3 +/- 1.3 ng/ml; week 4, 10.9 +/- 1.3 ng/ml). sICAM-1 and sELAM-1 were elevated at baseline but did not decrease during therapy. In the former group, free thyroxine and free triiodothyronine decreased faster. These data show that levels of sIL-2R in serum, but not those of sICAM-1 and sELAM-1, may be of clinical use in the early follow-up evaluation of medically treated patients.

Smallridge, R C; Tsokos, G C; Burman, K D; Porter, L; Cranston, T; Sfikakis, P P; Solomon, B L

1997-01-01

281

Soluble adhesion molecules as markers for sepsis and the potential pathophysiological discrepancy in neonates, children and adults.  

PubMed

Sepsis is a severe and life-threatening systemic inflammatory response to infection that affects all populations and age groups. The pathophysiology of sepsis is associated with aberrant interaction between leukocytes and the vascular endothelium. As inflammation progresses, the adhesion molecules that mediate these interactions become shed from cell surfaces and accumulate in the blood as soluble isoforms that are being explored as potential prognostic disease biomarkers. We critically review the studies that have tested the predictive value of soluble adhesion molecules in sepsis pathophysiology with emphasis on age, as well as the underlying mechanisms and potential roles for inflammatory shedding. Five soluble adhesion molecules are associated with sepsis, specifically, E-selectin, L-selectin and P-selectin, intercellular adhesion molecule-1 and vascular cell adhesion molecule-1. While increased levels of these soluble adhesion molecules generally correlate well with the presence of sepsis, their degree of elevation is still poorly predictive of sepsis severity scores, outcome and mortality. Separate analyses of neonates, children and adults demonstrate significant age-dependent discrepancies in both basal and septic levels of circulating soluble adhesion molecules. Additionally, a range of both clinical and experimental studies suggests protective roles for adhesion molecule shedding that raise important questions about whether these should positively or negatively correlate with mortality. In conclusion, while predictive properties of soluble adhesion molecules have been researched intensively, their levels are still poorly predictive of sepsis outcome and mortality. We propose two novel directions for improving clinical utility of soluble adhesion molecules: the combined simultaneous analysis of levels of adhesion molecules and their sheddases; and taking age-related discrepancies into account. Further attention to these issues may provide better understanding of sepsis pathophysiology and increase the usefulness of soluble adhesion molecules as diagnostic and predictive biomarkers. PMID:24602331

Zonneveld, Rens; Martinelli, Roberta; Shapiro, Nathan I; Kuijpers, Taco W; Plötz, Frans B; Carman, Christopher V

2014-01-01

282

Soluble adhesion molecules as markers for sepsis and the potential pathophysiological discrepancy in neonates, children and adults  

PubMed Central

Sepsis is a severe and life-threatening systemic inflammatory response to infection that affects all populations and age groups. The pathophysiology of sepsis is associated with aberrant interaction between leukocytes and the vascular endothelium. As inflammation progresses, the adhesion molecules that mediate these interactions become shed from cell surfaces and accumulate in the blood as soluble isoforms that are being explored as potential prognostic disease biomarkers. We critically review the studies that have tested the predictive value of soluble adhesion molecules in sepsis pathophysiology with emphasis on age, as well as the underlying mechanisms and potential roles for inflammatory shedding. Five soluble adhesion molecules are associated with sepsis, specifically, E-selectin, L-selectin and P-selectin, intercellular adhesion molecule-1 and vascular cell adhesion molecule-1. While increased levels of these soluble adhesion molecules generally correlate well with the presence of sepsis, their degree of elevation is still poorly predictive of sepsis severity scores, outcome and mortality. Separate analyses of neonates, children and adults demonstrate significant age-dependent discrepancies in both basal and septic levels of circulating soluble adhesion molecules. Additionally, a range of both clinical and experimental studies suggests protective roles for adhesion molecule shedding that raise important questions about whether these should positively or negatively correlate with mortality. In conclusion, while predictive properties of soluble adhesion molecules have been researched intensively, their levels are still poorly predictive of sepsis outcome and mortality. We propose two novel directions for improving clinical utility of soluble adhesion molecules: the combined simultaneous analysis of levels of adhesion molecules and their sheddases; and taking age-related discrepancies into account. Further attention to these issues may provide better understanding of sepsis pathophysiology and increase the usefulness of soluble adhesion molecules as diagnostic and predictive biomarkers.

2014-01-01

283

Soluble E-selectin and soluble ICAM-1 levels as markers of the activity of atopic dermatitis in children  

Microsoft Academic Search

The expression of adhesion molecules is up-regulated in the skin of atopic dermatitis (AD) patients, and the levels of the soluble adhesion molecules sE-selectin and sICAM-1 have been reported to reflect the endothelial activation in the skin of AD patients. The objective of the study was to investigate the relationship between symptom score and levels of sE-selectin, sICAM-1 and sVCAM-1

Albert Wolkerstorfer; Huub F. J. Savelkoul; Waard van der Spek de F. B; Herman J. Neijens; Tim van Meurs; Arnold P. Oranje

2003-01-01

284

Stuck on You: Adhesion  

NSDL National Science Digital Library

Learners explore water adhesion and learn about why water molecules are more strongly attracted to some substances than others. In an investigation titled "Fabric Frenzy," learners use a magnifying glass to examine different fabrics and hypothesize whether each kind would be good for soaking up water. Learners then weigh the dry fabrics, predict how water will affect the weight of each sample, wet the samples, and weigh them again to see how much water they in fact absorb. Learners also examine other liquids and compare their adhesion to water adhesion.

Jersey, New; Center, Liberty S.; Coalition, New J.

2006-01-01

285

Adhesive Contact Sweeper  

NASA Technical Reports Server (NTRS)

Adhesive contact sweeper removes hair and particles vacuum cleaner leaves behind, without stirring up dust. Also cleans loose rugs. Sweeper holds commercially available spools of inverted adhesive tape. Suitable for use in environments in which air kept free of dust; optics laboratories, computer rooms, and areas inhabited by people allergic to dust. For carpets, best used in tandem with vacuum cleaner; first pass with vacuum cleaner removes coarse particles, and second pass with sweeper extracts fine particles. This practice extends useful life of adhesive spools.

Patterson, Jonathan D.

1993-01-01

286

Mechanisms underlying neutrophil adhesion to apical epithelial membranes.  

PubMed Central

Crypt abscesses allow prolonged apposition of activated neutrophils to the epithelial surface of the colon. Adhesion of neutrophils to both the vascular endothelium and basolateral epithelial membrane share common effector molecules but are distinct processes. This study aimed to define the mechanisms that effect adhesion, independent of transmigration, to the apical epithelium. HT29 (cl 19A) cells were grown to confluency and incubated with neutrophils under conditions of: (i) neutrophil stimulation with phorbol-myristate-acetate; (ii) monolayer stimulation with interferon gamma, tumour necrosis factor alpha (IFN gamma, TNF alpha); and (iii) recent epithelial cell trypsinisation. These experiments were carried out in the presence of neutralising antibodies to CD18, CD11b, LFA-1, E-selectin, P-selectin, intracellular adhesion molecule 1 (ICAM-1), and ICAM-2; a novel CD11b/CD18 antagonist, neutrophil inhibitory factor (rNIF); adenosine receptor agonists (5'N-ethycarboxamido adenosine/N6-cylopentyladenosine (NECA/CPA)) and a platelet activating factor (PAF) receptor antagonist lexipafant. Adhesion of stimulated neutrophils to resting monolayers was Mac-1, CD18 dependent and ICAM-1, ICAM-2, E-selectin, P-selectin, PAF independent. Cytokine activated monolayers exhibited higher binding of neutrophils which was inhibited by rNIF and aCD18. Recently trypsinised monolayers bound neutrophils in a CD11b/CD18 and CD18 independent manner. Adenosine agonists failed to influence neutrophil adhesion under any condition. This study shows neutrophil adhesion to apical epithelial membranes is similar to that at the epithelial basolateral membrane, though different to that seen at the vascular endothelium. These results highlight regional differences in neutrophil adhesion molecule usage.

Meenan, J; Mevissen, M; Monajemi, H; Radema, S A; Soule, H R; Moyle, M; Tytgat, G N; van Deventer, S J

1996-01-01

287

Underwater adhesion: The barnacle way  

Microsoft Academic Search

Barnacle cement is an underwater adhesive insoluble protein complex. Marine proteins secreted by the invertebrates such as barnacles and mussels have potential application as powerful adhesives as they insolubilize and adhere to variety of substrates in aqueous environment. The adhesive properties of the barnacle adhesive proteins have been utilized for various dental and medical purposes. These polyphenolic proteins are currently

Lidita Khandeparker; Arga Chandrashekhar Anil

2007-01-01

288

Adhesion of Lunar Dust  

NASA Astrophysics Data System (ADS)

This paper reviews the physical characteristics of lunar dust and the effects of various fundamental forces acting on dust particles on surfaces in a lunar environment. There are transport forces and adhesion forces after contact. Mechanical forces (i.e., from rover wheels, astronaut boots and rocket engine blast) and static electric effects (from UV photo-ionization and/or tribo-electric charging) are likely to be the major contributors to the transport of dust particles. If fine regolith particles are deposited on a surface, then surface energy-related (e.g., van der Walls) adhesion forces and static-electric-image forces are likely to be the strongest contributors to adhesion. Some measurement techniques are offered to quantify the strength of adhesion forces. And finally some dust removal techniques are discussed.

Walton, Otis R.

2007-04-01

289

High Temperature Adhesive Systems.  

National Technical Information Service (NTIS)

Projected requirements for future high-performance jet engine, missile, and fighter aircraft structures will necessitate extensive use of high temperature structural adhesives. For example, many advanced jet engine and tactical aircraft components will ne...

E. H. Catsiff T. K. Dougherty W. E. Elias D. J. Vachon G. Angsten

1989-01-01

290

Adhesion of Lunar Dust  

NASA Technical Reports Server (NTRS)

This paper reviews the physical characteristics of lunar dust and the effects of various fundamental forces acting on dust particles on surfaces in a lunar environment. There are transport forces and adhesion forces after contact. Mechanical forces (i.e., from rover wheels, astronaut boots and rocket engine blast) and static electric effects (from UV photo-ionization and/or tribo-electric charging) are likely to be the major contributors to the transport of dust particles. If fine regolith particles are deposited on a surface, then surface energy-related (e.g., van der Walls) adhesion forces and static-electric-image forces are likely to be the strongest contributors to adhesion. Some measurement techniques are offered to quantify the strength of adhesion forces. And finally some dust removal techniques are discussed.

Walton, Otis R.

2007-01-01

291

Elastomer Toughened Polyimide Adhesives.  

National Technical Information Service (NTIS)

A rubber toughened addition type polyimide composition having excellent high temperature bonding characteristics in the fully cured state and improved peel strength and adhesive fracture resistance physical property characteristics is disclosed. The proce...

A. K. St.Clair T. L. St.Clair

1983-01-01

292

Adhesion of Lunar Dust.  

National Technical Information Service (NTIS)

This paper reviews the physical characteristics of lunar dust and the effects of various fundamental forces acting on dust particles on surfaces in a lunar environment. There are transport forces and adhesion forces after contact. Mechanical forces (i.e.,...

O. R. Walton

2007-01-01

293

Adhesion of Colloidal Particles.  

National Technical Information Service (NTIS)

The work presented shows that the development of experimental methods for determining adhesion forces in vacuo in the non-retarded case, has reached a high degree of sophistication. The measuring results obtained can be interpreted quantitatively in terms...

J. Visser

1973-01-01

294

Optical adhesive property study  

SciTech Connect

Tests were performed to characterize the mechanical and thermal properties of selected optical adhesives to identify the most likely candidate which could survive the operating environment of the Direct Optical Initiation (DOI) program. The DOI system consists of a high power laser and an optical module used to split the beam into a number of channels to initiate the system. The DOI requirements are for a high shock environment which current military optical systems do not operate. Five candidate adhesives were selected and evaluated using standardized test methods to determine the adhesives` physical properties. EC2216, manufactured by 3M, was selected as the baseline candidate adhesive based on the test results of the physical properties.

Sundvold, P.D.

1996-01-01

295

A role for cell adhesion in beryllium-mediated lung disease  

SciTech Connect

Chronic beryllium disease (CBD) is a debilitating lung disorder in which exposure to the lightweight metal beryllium (Be) causes the accumulation of beryllium-specific CD4+ T cells in the lung and formation of noncaseating pulmonary granulomas. Treatment for CBD patients who exhibit progressive pulmonary decline is limited to systemic corticosteroids, which suppress the severe host inflammatory response. Studies in the past several years have begun to highlight cell-cell adhesion interactions in the development of Be hypersensitivity and CBD. In particular, the high binding affinity between intercellular adhesion molecule 1 (I-CAM1) on lung epithelial cells and the {beta}{sub 2} integrin LFA-1 on migrating lymphocytes and macrophages regulates the concerted rolling of immune cells to sites of inflammation in the lung. In this review, we discuss the evidence that implicates cell adhesion processes in onset of Be disease and the potential of cell adhesion as an intervention point for development of novel therapies.

Hong-geller, Elizabeth [Los Alamos National Laboratory

2008-01-01

296

The focal adhesion kinase inhibitor PF-562,271 impairs primary CD4+ T cell activation.  

PubMed

The focal adhesion kinase inhibitor, PF-562,271, is currently in clinical development for cancer, however it is not known how PF-562,271 affects T cell function. Here, we demonstrate inhibitory effects of PF-562,271 on the activation of primary human and mouse T cells. PF-562,271 inhibits T cell receptor signaling-induced T cell adhesion to intercellular adhesion molecule-1 and T cell interactions with antigen-presenting cells. An additional focal adhesion kinase inhibitor, PF-573,228, and genetic depletion of focal adhesion kinase also impair T cell conjugation with antigen-presenting cells. PF-562,271 blocks phosphorylation of the signaling molecules zeta chain associate protein of 70 kDa, linker of activated T cells, and extracellular signal-regulated kinase, and impairs T cell proliferation. The effects observed on T cell proliferation cannot solely be attributed to focal adhesion kinase inhibition, as genetic depletion did not alter proliferation. The effect of PF-562,271 on T cell proliferation is not rescued when proximal T cell receptor signaling is bypassed by stimulation with phorbol-12-myristate-13-acetate and ionomycin. Taken together, our findings demonstrate that focal adhesion kinase regulates integrin-mediated T cell adhesion following T cell receptor activation. Moreover, our findings suggest that PF-562,271 may have immunomodulatory effects that could impact its therapeutic applications. PMID:23928188

Wiemer, Andrew J; Wernimont, Sarah A; Cung, Thai-Duong; Bennin, David A; Beggs, Hilary E; Huttenlocher, Anna

2013-09-15

297

Knockdown of stromal interaction molecule 1 attenuates hepatocyte growth factor-induced endothelial progenitor cell proliferation.  

PubMed

Increased Ca(2+) entry through store-operated Ca(2+) channels (SOCCs) plays an essential role in the regulation of hepatocyte growth factor (HGF)-induced cell proliferation. Stromal interaction molecule 1 (STIM1) is thought to transmit endoplasmic reticulum (ER) Ca(2+) store depletion signals to the plasma membrane (PM), causing the opening of SOCCs in the PM. However, the relationship between HGF and STIM1 in endothelial progenitor cell (EPC) proliferation remains uncharacterized. The objective of this study was to evaluate the potential involvement of STIM1 in HGF-induced EPC proliferation. For this purpose, we used cultured rat bone marrow-derived EPCs and found that HGF-induced EPC proliferation at low concentrations. Store-operated Ca(2+) entry (SOCE) was elevated in HGF-treated EPCs, and the SOCC inhibitors 2-aminoethoxydiphenyl borate (2-APB) and BTP-2 inhibited the HGF-induced proliferation response. Moreover, STIM1 mRNA and protein expression levels were increased in response to HGF stimulation and knockdown of STMI1 decreased SOCE and prevented HGF-induced EPC proliferation. In conclusion, our data suggest that HGF-induced EPC proliferation is mediated partly via activation of STIM1. PMID:20404049

Shi, Yankun; Song, Mingbao; Guo, Ruiwei; Wang, Hong; Gao, Pan; Shi, Weibin; Huang, Lan

2010-03-01

298

Accelerated receptor shedding inhibits kidney injury molecule-1 (KIM-1)-mediated efferocytosis.  

PubMed

Efficient clearance of apoptotic cells (efferocytosis) prevents inflammation and permits repair following tissue injury. Kidney injury molecule-1 (KIM-1) is a receptor for phosphatidylserine, an "eat-me" signal exposed on the surface of apoptotic cells that marks them for phagocytic clearance. KIM-1 is upregulated on proximal tubule epithelial cells (PTECs) during ischemic acute kidney injury (AKI), enabling efferocytosis by surviving PTECs. KIM-1 is spontaneously cleaved at its ectodomain region to generate a soluble fragment that serves a sensitive and specific biomarker for AKI, but the biological relevance of KIM-1 shedding is unknown. Here, we sought to determine how KIM-1 shedding might regulate efferocytosis. Using cells that endogenously and exogenously express KIM-1, we found that hydrogen peroxide-mediated oxidative injury or PMA treatment accelerated KIM-1 shedding in a dose-dependent manner. KIM-1 shedding was also accelerated when apoptotic cells were added. Accelerated shedding or the presence of excess soluble KIM-1 in the extracellular milieu significantly inhibited efferocytosis. We also identified that TNF-?-converting enzyme (TACE or ADAM17) mediates both the spontaneous and PMA-accelerated shedding of KIM-1. While accelerated shedding inhibited efferocytosis, we found that spontaneous KIM-1 cleavage does not affect the phagocytic efficiency of PTECs. Our results suggest that KIM-1 shedding is accelerated by worsening cellular injury, and excess soluble KIM-1 competitively inhibits efferocytosis. These findings may be important in AKI when there is severe cellular injury. PMID:24829508

Gandhi, Rushi; Yi, James; Ha, Jihyen; Shi, Hang; Ismail, Ola; Nathoo, Sahra; Bonventre, Joseph V; Zhang, Xizhong; Gunaratnam, Lakshman

2014-07-15

299

Kidney injury molecule-1: more than just an injury marker of tubular epithelial cells?  

PubMed

Regardless of the original causes and etiology, the progression to renal function declines follows a final common pathway associated with tubulointerstitial injury, in which the proximal tubular epithelial cells (PTEC) are instrumental. Kidney injury molecule-1 (KIM-1) is an emerging biomarker, and its expression and release are induced in PTEC upon injury. KIM-1 plays the role as a double-edged sword and implicates in the process of kidney injury and healing. Expression of KIM-1 is also associated with tubulointerstitial inflammation and fibrosis. More importantly, KIM-1 expressing PTEC play the role as the residential phagocytes, contribute to the removal of apoptotic cells and facilitate the regeneration of injured tubules. The precise mechanism of KIM-1 and its sheded ectodomain on restoration of tubular integrity after injury is not fully understood. Other than PTEC, macrophages (Mø) also implicate in tubular repair. Understanding the crosstalk between Mø and the injured PTEC is essential for designing appropriate methods for controlling the sophisticated machinery in tubular regeneration and healing. This article will review the current findings of KIM-1, beginning with its basic structure, utility as a biomarker, and possible functions, with focus on the role of KIM-1 in regeneration and healing of injured PTEC. PMID:23086807

Lim, Ai Ing; Tang, Sydney C W; Lai, Kar Neng; Leung, Joseph C K

2013-05-01

300

Chronic epithelial kidney injury molecule-1 expression causes murine kidney fibrosis.  

PubMed

Acute kidney injury predisposes patients to the development of both chronic kidney disease and end-stage renal failure, but the molecular details underlying this important clinical association remain obscure. We report that kidney injury molecule-1 (KIM-1), an epithelial phosphatidylserine receptor expressed transiently after acute injury and chronically in fibrotic renal disease, promotes kidney fibrosis. Conditional expression of KIM-1 in renal epithelial cells (Kim1(RECtg)) in the absence of an injury stimulus resulted in focal epithelial vacuolization at birth, but otherwise normal tubule histology and kidney function. By 4 weeks of age, Kim1(RECtg) mice developed spontaneous and progressive interstitial kidney inflammation with fibrosis, leading to renal failure with anemia, proteinuria, hyperphosphatemia, hypertension, cardiac hypertrophy, and death, analogous to progressive kidney disease in humans. Kim1(RECtg) kidneys had elevated expression of proinflammatory monocyte chemotactic protein-1 (MCP-1) at early time points. Heterologous expression of KIM-1 in an immortalized proximal tubule cell line triggered MCP-1 secretion and increased MCP-1-dependent macrophage chemotaxis. In mice expressing a mutant, truncated KIM-1 polypeptide, experimental kidney fibrosis was ameliorated with reduced levels of MCP-1, consistent with a profibrotic role for native KIM-1. Thus, sustained KIM-1 expression promotes kidney fibrosis and provides a link between acute and recurrent injury with progressive chronic kidney disease. PMID:23979159

Humphreys, Benjamin D; Xu, Fengfeng; Sabbisetti, Venkata; Grgic, Ivica; Naini, Said Movahedi; Wang, Ningning; Chen, Guochun; Xiao, Sheng; Patel, Dhruti; Henderson, Joel M; Ichimura, Takaharu; Mou, Shan; Soeung, Savuth; McMahon, Andrew P; Kuchroo, Vijay K; Bonventre, Joseph V

2013-09-01

301

Dry adhesives with sensing features  

NASA Astrophysics Data System (ADS)

Geckos are capable of detecting detachment of their feet. Inspired by this basic observation, a novel functional dry adhesive is proposed, which can be used to measure the instantaneous forces and torques acting on an adhesive pad. Such a novel sensing dry adhesive could potentially be used by climbing robots to quickly realize and respond appropriately to catastrophic detachment conditions. The proposed torque and force sensing dry adhesive was fabricated by mixing Carbon Black (CB) and Polydimethylsiloxane (PDMS) to form a functionalized adhesive with mushroom caps. The addition of CB to PDMS resulted in conductive PDMS which, when under compression, tension or torque, resulted in a change in the resistance across the adhesive patch terminals. The proposed design of the functionalized dry adhesive enables distinguishing an applied torque from a compressive force in a single adhesive pad. A model based on beam theory was used to predict the change in resistance across the terminals as either a torque or compressive force was applied to the adhesive patch. Under a compressive force, the sensing dry adhesive was capable of measuring compression stresses from 0.11 Pa to 20.9 kPa. The torque measured by the adhesive patch ranged from 2.6 to 10 mN m, at which point the dry adhesives became detached. The adhesive strength was 1.75 kPa under an applied preload of 1.65 kPa for an adhesive patch with an adhesive contact area of 7.07 cm2.

Krahn, J.; Menon, C.

2013-08-01

302

hsCRP, sICAM-1 and TAFI in Hemodialysis Patients: Linking Inflammation and Hypofibrinolysis to Cardiovascular Events  

Microsoft Academic Search

Background\\/Aims: Growing evidence suggests that inflammation, oxidative stress and hypofibrinolysis may have a pivotal role in the high prevalence of cardiovascular disease (CVD) in chronic kidney disease (CKD) patients. This study aims to investigate the association of these processes with the incidence of CVD in hemodialysis (HD) patients and to examine the modulating effect of oral L-arginine in HD patients

Mohamed Z. Gad; Hala O. El-Mesallamy; Eman F. Sanad

2008-01-01

303

Regulation and function of adhesion molecule expression by human alveolar epithelial cells.  

PubMed Central

The role of major histocompatibility complex (MHC) and adhesion molecule expression by alveolar epithelium on the modulation of immune responses in the lung is not understood. We have developed efficient methods to isolate, purify and culture human alveolar epithelial cells (type II pneumocytes) in vitro. The expression of MHC and adhesion molecules by isolated, cultured and cytokine-stimulated alveolar epithelial cells was quantified by flow cytometry, and demonstrated the presence of T-cell ligands including class I MHC, HLA-DR and HLA-DP, intracellular adhesion molecule-1 (ICAM-1; CD54) and lymphocyte function-associated antigen (LFA-3; CD58), but not vascular cell adhesion molecule-1 (VCAM-1) (CD106) or B7 (CD80). The proinflammatory cytokine interferon-gamma (IFN-gamma) caused an up-regulation of class I MHC and ICAM-1. In contrast, tumour necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) had little effect on the expression of these surface antigens by human alveolar epithelial cells. The functional activity of alveolar epithelial adhesion molecules was then studied by determining their ability to bind allogeneic lymphocytes. An increase in lymphocyte adherence to monolayers of alveolar epithelial cells was observed following in vitro activation. However, up-regulation of alveolar epithelial counter receptors with the proinflammatory cytokine gamma-IFN did not enhance adhesion. The adhesive interaction between CD18 on lymphocytes and ICAM-1 on alveolar epithelial cells was demonstrated by the use of blocking antibodies specific for both ligands. Blockade of LFA-3 on alveolar monolayers also suppressed lymphocyte adherence. In conclusion, alveolar epithelial cells expressed MHC HLA-A, B, C, HLA-DR and -DP, and functional adhesion molecules including ICAM-1 and LFA-3. Images Figure 1 Figure 2 Figure 4

Cunningham, A C; Kirby, J A

1995-01-01

304

Monosialic ganglioside GM3 specifically suppresses the monocyte adhesion to endothelial cells for inflammation.  

PubMed

Vascular endothelial growth factor (VEGF) is well known as a significant angiogenic factor, and also functions as a proinflammatory cytokine, which induces adhesion of leukocyte to endothelial cells in inflammation reaction. In this study, we show that ganglioside GM3 inhibits the VEGF-induced expression of intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) through activation of nuclear factor-?B (NF-?B) via protein kinase B (AKT) signaling in human umbilical vein endothelial cells (HUVECs), relating with leukocyte recruitment to endothelial cells under inflammatory conditions. In addition, ganglioside GM3 significantly reduced the monocyte adhesion to HUVECs as determined by the monolayer cell adhesion assay. Furthermore, in VEGF-injected mice for the inflammatory condition, ganglioside GM3 markedly decreased the expression of ICAM-1 and VCAM-1 in vein tissues. These results suggest that ganglioside GM3 has an anti-inflammatory role by suppressing the expression of inflammatory-related molecules during in vitro and in vivo inflammation. PMID:24120649

Kim, Seok-Jo; Chung, Tae-Wook; Choi, Hee-Jung; Jin, Un-Ho; Ha, Ki-Tae; Lee, Young-Choon; Kim, Cheorl-Ho

2014-01-01

305

Downregulation of Carcinoembryonic Antigen-Related Cell Adhesion Molecule 1 in Oral Squamous Cell Carcinoma: Correlation with Tumor Progression and Poor Prognosis  

Microsoft Academic Search

Objective: To identify genes associated with therapeutic targets of oral squamous cell carcinoma (OSCC), we compared gene expression profiles in OSCC-derived cell lines with human normal oral keratinocytes. Methods: We analyzed the gene expression profiles of OSCCs using Affymetrix GeneChip analysis. The identified genes were analyzed by an Ingenuity Pathway Analysis tool to identify networks of interacting genes. A candidate

Keiji Shinozuka; Katsuhiro Uzawa; Kazuaki Fushimi; Yukio Yamano; Masashi Shiiba; Hiroki Bukawa; Hidetaka Yokoe; Hideki Tanzawa

2009-01-01

306

Vascular cell adhesion molecule-1 (CD106) is cleaved by neutrophil proteases in the bone marrow following hematopoietic progenitor cell mobilization by granulocyte colony-stimulating factor  

Microsoft Academic Search

Mobilized progenitor cells currently repre- sent the most commonly used source of hematopoietic progenitor cells (HPCs) to effect hematopoietic reconstitution follow- ing myeloablative chemotherapies. De- spite their widespread use, the molecular mechanisms responsible for the enforced egress of HPCs from the bone marrow (BM) into the circulation in response to mobilizing agents such as cytokines re- main to be determined.

Jean-Pierre Levesque; Yasushi Takamatsu; Susan K. Nilsson; David N. Haylock; Paul J. Simmons

2001-01-01

307

Absence of Platelet Endothelial Cell Adhesion Molecule 1, PECAM-1/CD31, In Vivo Increases Resistance to Salmonella enterica Serovar Typhimurium in Mice  

PubMed Central

PECAM-1/CD31 is known to regulate inflammatory responses and exhibit pro- and anti-inflammatory functions. This study was designed to determine the functional role of PECAM-1 in susceptibility to murine primary in vivo infection with Salmonella enterica serovar Typhimurium and in in vitro inflammatory responses of peritoneal macrophages. Lectin profiling showed that cellular PECAM-1 and recombinant human PECAM-1-Ig chimera contain high levels of mannose sugars and N-acetylglucosamine. Consistent with this carbohydrate pattern, both recombinant human and murine PECAM-1-Ig chimeras were shown to bind S. Typhimurium in a dose-dependent manner in vitro. Using oral and fecal-oral transmission models of S. Typhimurium SL1344 infection, PECAM-1?/? mice were found to be more resistant to S. Typhimurium infection than wild-type (WT) C57BL/6 mice. While fecal shedding of S. Typhimurium was comparable in wild-type and PECAM-1?/? mice, the PECAM-1-deficient mice had lower bacterial loads in systemic organs such as liver, spleen, and mesenteric lymph nodes than WT mice, suggesting that extraintestinal dissemination was reduced in the absence of PECAM-1. This reduced bacterial load correlated with reduced tumor necrosis factor (TNF), interleukin-6 (IL-6), and monocyte chemoattractant protein (MCP) levels in sera of PECAM-1?/? mice. Following in vitro stimulation of macrophages with either whole S. Typhimurium, lipopolysaccharide (LPS) (Toll-like receptor 4 [TLR4] ligand), or poly(I·C) (TLR3 ligand), production of TNF and IL-6 by PECAM-1?/? macrophages was reduced. Together, these results suggest that PECAM-1 may have multiple functions in resistance to infection with S. Typhimurium, including binding to host cells, extraintestinal spread to deeper tissues, and regulation of inflammatory cytokine production by infected macrophages.

Lovelace, Michael D.; Yap, May Lin; Yip, Jana; Muller, William; Wijburg, Odilia

2013-01-01

308

Xia-Bai-San inhibits lipopolysaccharide-induced activation of intercellular adhesion molecule-1 and nuclear factor-kappa B in human lung cells  

Microsoft Academic Search

Xia-Bai-San (XBS) is a traditional Chinese medicine that has been used clinically for centuries in Asian countries to treat some types of common cold and asthma-like diseases similar to infantile pneumonia and childhood bronchitis. In previous studies, XBS was found to suppress the inflammatory process induced in lungs of mice treated with lipopolysaccharide (LPS).

Kuo-Hua Lee; Ming-Hsien Yeh; Shung-Te Kao; Che-Ming Hung; Bor-Chyuan Chen; Ching-Ju Liu; Chia-Chou Yeh

2009-01-01

309

Expression of adhesion molecules by Lp(a): a potential novel mechanism for its atherogenicity  

Microsoft Academic Search

Lp(a) is a major inherited risk factor for premature atherosclerosis. The mechanism of Lp(a) atherogenicity has not been elucidated, but likely involves both its ability to interfere with plas- minogen activation and its atherogenic potential as a lipoprotein particle after receptor-mediated uptake. We demonstrate that Lp(a) stimulates production of vascular cell adhesion molecule 1 (VCAM-1) and E- selectin in cultured

SEAN ALLEN; SHABEENA KHAN; SHUI-PANG TAM; MARLYS KOSCHINSKY; PATRICIA TAYLOR; MAGDI YACOUB

310

Flexibilized copolyimide adhesives  

NASA Technical Reports Server (NTRS)

Two copolyimides, LARC-STPI and STPI-LARC-2, with flexible backbones were processed and characterized as adhesives. The processability and adhesive properties were compared to those of a commercially available form of LARC-TPI. Lap shear specimens were fabricated using adhesive tape prepared from each of the three polymers. Lap shear tests were performed at room temperature, 177 C, and 204 C before and after exposure to water-boil and to thermal aging at 204 C for up to 1000 hours. The three adhesive systems possess exceptional lap shear strengths at room temperature and elevated temperatures both before and after thermal exposure. LARC-STPI, because of its high glass transition temperature provided high lap shear strengths up to 260 C. After water-boil, LARC-TPI exhibited the highest lap shear strengths at room temperature and 177 C, whereas the LARC-STPI retained a higher percentage of its original strength when tested at 204 C. These flexible thermoplastic copolyimides show considerable potential as adhesives based on this study and because of the ease of preparation with low cost, commercially available materials.

Progar, Donald J.; St.clair, Terry L.

1988-01-01

311

Platelet Adhesion under Flow  

PubMed Central

Platelet adhesive mechanisms play a well-defined role in hemostasis and thrombosis, but evidence continues to emerge for a relevant contribution to other pathophysiological processes including inflammation, immune-mediated responses to microbial and viral pathogens, and cancer metastasis. Hemostasis and thrombosis are related aspects of the response to vascular injury, but the former protects from bleeding after trauma while the latter is a disease mechanism. In either situation, adhesive interactions mediated by specific membrane receptors support the initial attachment of single platelets to cellular and extracellular matrix constituents of the vessel wall and tissues. In the subsequent steps of thrombus growth and stabilization, adhesive interactions mediate platelet to platelet cohesion (aggregation) and anchoring to the fibrin clot. A key functional aspect of platelets is their ability to circulate in a quiescent state surveying the integrity of the inner vascular surface, coupled to a prompt reaction wherever alterations are detected. In many respects, therefore, platelet adhesion to vascular wall structures, to one another or to other blood cells are facets of the same fundamental biological process. The adaptation of platelet adhesive functions to the effects of blood flow is the main focus of this review.

Ruggeri, Zaverio M.

2011-01-01

312

Differential effects of isoflurane and CO2 inhalation on plasma levels of inflammatory markers associated with collagen-induced arthritis in DBA mice.  

PubMed

Inhalation of CO2 or isoflurane is a commonly used method of euthanasia with mice, but information related to their effects on serum inflammatory markers in chronic models of inflammation is limited. In the current study, nineteen-week old DBA female mice with (n = 53) or without (n = 51) collagen-induced arthritis were randomly assigned to euthanization with CO2 (n = 55) or isoflurane (n = 49. Plasma was collected for the measurement of soluble intercellular adhesion molecule-1 (sICAM-1), tumor necrosis factor alpha (TNF-alpha), and interleukin-6 (IL-6) by ELISA. When mice without and with collagen-induced arthritis were pooled, compared to CO2, administration of isoflurane was associated with lower production of the pro-inflammatory cytokines TNF-alpha (pg/ml, mean +/- SEM) (26.1 +/- 2.82 versus 48.1 +/- 7.99) and IL-6 (25.18 +/- 2.73 versus 48.1 +/- 6.82) (ANOVA, p < 0.05). In contrast to TNF-alpha and IL-6, administration of CO2 decreased the plasma sICAM-1 level (1170+/- 50 versus 758 +/- 24 for CO2) (p < 0.00001). When data were analyzed as a function of collagen-induced arthritis, the differences between CO2 and isoflurane persisted. Low plasma sICAM-1 levels found in CO2 euthanasia group may be due to degradation. Since mice are the most common animal model for studying inflammation, researchers should be aware of these iatrogenic experimental variables before interpreting their data. PMID:19341822

Lawrance, Christopher C; Lucas, Edralin A; Clarke, Stephen L; Smith, Brenda J; Kuvibidila, Solo

2009-07-01

313

Diagnostic Value of Urinary Kidney Injury Molecule 1 for Acute Kidney Injury: A Meta-Analysis  

PubMed Central

Background Urinary Kidney Injury Molecule 1 (KIM-1) is a proximal tubular injury biomarker for early detection of acute kidney injury (AKI), with variable performance characteristics depending on clinical and population settings. Methods Meta-analysis was performed to assess the diagnostic value of urinary KIM-1 in AKI. Relevant studies were searched from MEDLINE, EMBASE, Pubmed, Elsevier Science Direct, Scopus, Web of Science, Google Scholar and Cochrane Library. Meta-analysis methods were used to pool sensitivity and specificity and to construct summary receiver operating characteristic (SROC) curves. Results A total of 2979 patients from 11 eligible studies were enrolled in the analysis. Five prospective cohorts, two cross-sectional and four case-control studies were identified for meta-analysis. The estimated sensitivity of urinary KIM-1 for the diagnosis of AKI was 74.0% (95% CI, 61.0%–84.0%), and specificity was 86.0% (95% CI, 74.0%–93.0%). The SROC analysis showed an area under the curve of 0.86(0.83–0.89). Subgroup analysis suggested that population settings and detection time were the key factors affecting the efficiency of KIM-1 for AKI diagnosis. Limitation Various population settings, different definition of AKI and Serum creatinine level used as the standard might have influence on AKI diagnosis. The relatively small number of studies and heterogeneity between them also affected the evaluation. Conclusion Urinary KIM-1 may be a promising biomarker for early detection of AKI with considerable predictive value, especially for cardiac surgery patients, and its potential value needs to be validated in large studies and across a broader scope of clinical settings.

Xu, Weijia; Zhang, Zhen; Wang, Chunlin; Qi, Chaojun; Ni, Zhaohui; Mou, Shan

2014-01-01

314

Effect of treatment on urinary kidney injury molecule-1 in IgA nephropathy  

PubMed Central

Background Kidney injury molecule-1 (KIM-1) is a biomarker useful for detecting early tubular damage and has been recently reported as a useful marker for evaluating kidney injury in IgA nephropathy (IgAN). We therefore investigated whether treatment decreases urinary KIM-1 excretion in IgAN. Methods We prospectively enrolled 37 patients with biopsy-proven IgAN. Urinary KIM-1 was assessed before and after treatment, which included low salt diet, blood pressure control, pharmacotherapy with angiotensin receptor blockers and/or angiotensin converting enzyme inhibitors, and immunosuppressive agents as necessary. The median treatment duration was 24 months. Results Urinary KIM-1/creatinine (Cr) was significantly decreased in patients with IgAN after treatment compared to baseline (P?

2013-01-01

315

Propofol protects against high glucose-induced endothelial adhesion molecules expression in human umbilical vein endothelial cells  

PubMed Central

Background Hyperglycemia could induce oxidative stress, activate transcription factor nuclear factor kappa B (NF-?B), up-regulate expression of endothelial adhesion molecules, and lead to endothelial injury. Studies have indicated that propofol could attenuate oxidative stress and suppress NF-?B activation in some situations. In the present study, we examined whether and how propofol improved high glucose-induced up-regulation of endothelial adhesion molecules in human umbilical vein endothelial cells (HUVECs). Methods Protein expression of endothelial adhesion molecules, NF-?B, inhibitory subunit of NF-?B? (I?B?), protein kinase C?2 (PKC?2), and phosphorylation of PKC?2 (Ser660) were measured by Western blot. NF-?B activity was measured by electrophoretic mobility shift assay. PKC activity was measured with SignaTECT PKC assay system. Superoxide anion (O2.-) accumulation was measured with the reduction of ferricytochrome c assay. Human peripheral mononuclear cells were prepared with Histopaque-1077 solution. Results High glucose induced the expression of endothelial selectin (E-selectin), intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and increased mononuclear-endothelial adhesion. High glucose induced O2.- accumulation, PKC?2 phosphorylation and PKC activation. Further, high glucose decreased I?B? expression in cytoplasm, increased the translocation of NF-?B from cytoplasm to nuclear, and induced NF-?B activation. Importantly, we found these high glucose-mediated effects were attenuated by propofol pretreatment. Moreover, CGP53353, a selective PKC?2 inhibitor, decreased high glucose-induced NF-?B activation, adhesion molecules expression, and mononuclear-endothelial adhesion. Conclusion Propofol, via decreasing O2.- accumulation, down-regulating PKC?2 Ser660 phosphorylation and PKC as well as NF-?B activity, attenuated high glucose-induced endothelial adhesion molecules expression and mononuclear-endothelial adhesion.

2013-01-01

316

Adhesion in Nanodiamond Particles  

NASA Astrophysics Data System (ADS)

Due to their excellent mechanical properties and biologically non-toxic nature, nanodiamonds show great promise for applications in tribology, lubrication, drug delivery, tissue scaffolds and surgical implants. In order to design effective nanocomposites and other biomedical systems exploiting these properties, it is important to understand the properties and mechanisms by which nanodiamonds adhere to other materials, and how they behave at interfaces. In this article, the adhesive force between nanodiamond particles and the silicon scanning probe microscope tip are reported. The adhesive force can be correlated to the purity and functionalization of nanodiamond surface, and the values range from 0.1nN to 2.0nN for the samples studied. It is observed that the lateral forces applied by the scanning probe tip can cause the adhesive forces to increase by an order of magnitude from 0.1 to 2.0nN at regions where the tip experiences maximum contact force.

Rao Aravind, Vasudeva; Lutkus, Luke; Legum, Benjamin

2013-03-01

317

Pathophysiology of adhesions.  

PubMed

Formation of intraperitoneal adhesions after abdominal orpelvic surgery is a very common phenomenon. Although thereis no universally accepted definition, they are bridges of scartissue between the various organs of the peritoneal cavity as aresult of a local repair process excessively. Adhesions can becongenital or acquired as a local inflammatory process. Someadhesions can be asymptomatic, but many of them can causesevere complications such as abdominal or pelvic pain, femaleinfertility, and intestinal obstruction. Physicians and patientsshould be informed of the possibility of postoperative intraperitonealadhesions and this possibility should be mentioned inthe informed consent signed by the patient. The formation ofadhesions has multiple proinflammatory mechanismsinvolved, many with a pathophysiology still incompleteunderstood. Laparoscopic procedures do not diminish muchthe possibility of developing postoperative adhesions.Diagnostic imaging is quite uncertain, and the possibilities ofpreventing with a poor final result. The use of correct surgicaltechnique and avoidance of traumatic intraperitoneal organsmaneuvers may help reduce postoperative adhesionsincidence. PMID:24956331

Bu?ureanu, Sa; Bu?ureanu, Tas

2014-01-01

318

Adhesive particle shielding  

DOEpatents

An efficient device for capturing fast moving particles has an adhesive particle shield that includes (i) a mounting panel and (ii) a film that is attached to the mounting panel wherein the outer surface of the film has an adhesive coating disposed thereon to capture particles contacting the outer surface. The shield can be employed to maintain a substantially particle free environment such as in photolithographic systems having critical surfaces, such as wafers, masks, and optics and in the tools used to make these components, that are sensitive to particle contamination. The shield can be portable to be positioned in hard-to-reach areas of a photolithography machine. The adhesive particle shield can incorporate cooling means to attract particles via the thermophoresis effect.

Klebanoff, Leonard Elliott (Dublin, CA); Rader, Daniel John (Albuquerque, NM); Walton, Christopher (Berkeley, CA); Folta, James (Livermore, CA)

2009-01-06

319

Natural Underwater Adhesives  

PubMed Central

The general topic of this review is protein-based underwater adhesives produced by aquatic organisms. The focus is on mechanisms of interfacial adhesion to native surfaces and controlled underwater solidification of natural water-borne adhesives. Four genera that exemplify the broad range of function, general mechanistic features, and unique adaptations are discussed in detail: blue mussels, acorn barnacles, sandcastle worms, and freshwater caddisfly larva. Aquatic surfaces in nature are charged and in equilibrium with their environment, populated by an electrical double layer of ions as well as adsorbed natural polyelectrolytes and microbial biofilms. Surface adsorption of underwater bioadhesives likely occurs by exchange of surface bound ligands by amino acid sidechains, driven primarily by relative affinities and effective concentrations of polymeric functional groups. Most aquatic organisms exploit modified amino acid sidechains, in particular phosphorylated serines and hydroxylated tyrosines (dopa), with high-surface affinity that form coordinative surface complexes. After delivery to the surfaces as a fluid, permanent natural adhesives solidify to bear sustained loads. Mussel plaques are assembled in a manner superficially reminiscent of in vitro layer-by-layer strategies, with sequentially delivered layers associated through Fe(dopa)3 coordination bonds. The adhesives of sandcastle worms, caddisfly larva, and barnacles may be delivered in a form somewhat similar to in vitro complex coacervation. Marine adhesives are secreted, or excreted, into seawater that has a significantly higher pH and ionic strength than the internal environment. Empirical evidence suggests these environment triggers could provide minimalistic, fail-safe timing mechanisms to prevent premature solidification (insolubilization) of the glue within the secretory system, yet allow rapid solidification after secretion. Underwater bioadhesives are further strengthened by secondary covalent curing.

Stewart, Russell J.; Ransom, Todd C.; Hlady, Vladimir

2011-01-01

320

Elastomer toughened polyimide adhesives  

NASA Technical Reports Server (NTRS)

A rubber-toughened addition-type polyimide composition is disclosed which has excellent high temperature bonding characteristics in the fully cured state, and improved peel strength and adhesive fracture resistance physical property characteristics. The process for making the improved adhesive involves preparing the rubber containing amic acid prepolymer by chemically reacting an amine-terminated elastomer and an aromatic diamine with an aromatic dianhydride with which a reactive chain stopper anhydride was mixed, and utilizing solvent or mixture of solvents for the reaction.

St.clair, A. K.; St.clair, T. L. (inventors)

1983-01-01

321

Biomimetic Adhesive Polymers Based on Mussel Adhesive Proteins  

Microsoft Academic Search

Nature provides many outstanding examples of adhesive strategies from which chemists and material scientists can draw inspiration in their pursuit of new adhesive materials. As described in other chapters of this book, detailed studies of the adhesive mechanisms of geckos, mussels and other organisms during the past several decades have enhanced our understanding of the underlying physicochemical principles to the

BRUCE P. LEE; JEFFREY L. DALSIN; PHILLIP B. MESSERSMITH

322

Adhesive for cryogenic temperature applications  

NASA Technical Reports Server (NTRS)

Adhesive, which bonds a metal liner to a filament wound composite structure used for cryogenic pressure vessels, prevents the metal liner from buckling under depressurization. The adhesive consists of adducts of urethane and epoxy resins.

Doyle, H. M.

1969-01-01

323

Blockage of Cell Adhesion Molecules.  

National Technical Information Service (NTIS)

The invention relates, in general, to a method of blocking of cell adhesion molecules. In particular, the invention relates to a method of blocking cell adhesion molecules with monoclonal antibodies or synthesized substances.

S. M. Whitecup C. C. Chan R. B. Nussenblatt

1991-01-01

324

Effect of mechanical deformation of neutrophils on their CD18/ICAM-1-dependent adhesion.  

PubMed

Mechanical deformation of polymorphonuclear leukocytes (PMN) changes their expression of the surface adhesion molecule CD11b/CD18. We tested the hypothesis that mechanical deformation of PMN enhances their adhesiveness. Purified human PMN were deformed through either 5- or 3-microm polycarbonate membrane filters and allowed to adhere to 96-well plates coated with human recombinant intercellular adhesion molecule-1 (ICAM-1). Flow cytometric studies showed that deformation of PMN increased CD11b/CD18 expression (P < 0.01). PMN adhesion to ICAM-1-coated plates was dependent on the magnitude of cell deformation (5 microm, 63.8 +/- 8.1%, P < 0.04; 3 microm, 232.4 +/- 20.9%, P < 0.01). Priming of PMN (0.5 nM N-formyl-methionyl-leucyl-phenylalanine) before deformation (5 microm) increased PMN adhesion (63.8 +/- 8.1 vs. 105.3 +/- 16.4%; P < 0.04). Stimulation (5% zymosan-activated plasma) of PMN after deformation resulted in increased adhesion, and the degree of increase was dependent on the magnitude of PMN deformation (stimulation, 50.6 +/- 4%; 5-microm filtration and stimulation, 62.9 +/- 6.6%; 3-microm filtration and stimulation, 249.9 +/- 24.2%; P < 0.01). This study shows that mechanical deformation of PMN causes an increase in PMN adhesiveness to ICAM-1 that was enhanced by both priming of PMN before deformation and stimulation after cell deformation. PMID:11509502

Anderson, G J; Roswit, W T; Holtzman, M J; Hogg, J C; Van Eeden, S F

2001-09-01

325

Unique sensitivities to cytokine regulated expression of adhesion molecules in human heart-derived endothelial cells.  

PubMed

The expression of adhesion molecules by endothelial cells is crucial in many inflammatory processes and plays an active role in the development of reperfusion injury, acute and chronic rejection. The expression of adhesion molecules in different parts of the coronary tree to cytokine stimulation is not known. We describe here a detailed study of the effects of the inflammatory cytokines TNFalpha and IL-1beta on the expression of adhesion molecules vascular cell adhesion molecule-1 (VCAM-1), E-selectin and intracellular cell adhesion molecule-1 (ICAM-1) on human aortic root (HAEC), coronary artery (HCAEC) and heart microvascular (HHMEC)) endothelial cells in culture, using flow cytometry. We found constitutive levels of both VCAM-1 and E-Selectin on HCAEC and HHMEC (approximately 20%) which were significantly higher compared to HAEC (approximately 3%). There was an extreme sensitivity of HCAEC and HHMEC to 0.002 ng/ml TNFalpha: (VCAM-1 approximately 40%, E-Selectin approximately 25%) respectively, compared to HAEC (VCAM-1 approximately 5%, E-selectin approximately 5%). IL-1beta showed a similar pattern of expression at low doses (5 U/ml), but was less potent. We also observed prolonged expression of these adhesion molecules, especially on the HHMEC (>48 hours) compared to HAEC. There was also increased binding of peripheral blood mononuclear cells (PBMC) to both non-stimulated and TNFalpha stimulated HCAEC and HHMEC compared to HAEC. This data suggest that endothelial cells in different regions of the coronary tree express different patterns of basal and cytokine-stimulated adhesion molecule expression. PMID:11409849

McDouall, R M; Farrar, M W; Khan, S; Yacoub, M H; Allen, S P

2001-01-01

326

Osteoblast adhesion on nanophase ceramics  

Microsoft Academic Search

Osteoblast adhesion on nanophase alumina (Al2O3) and titania (TiO2) was investigated in vitro. Osteoblast adhesion to nanophase alumina and titania in the absence of serum from Dulbecco’s modified Eagle medium (DMEM) was significantly (P<0.01) less than osteoblast adhesion to alumina and titania in the presence of serum. In the presence of 10% fetal bovine serum in DMEM osteoblast adhesion on

Thomas J Webster; Richard W Siegel; Rena Bizios

1999-01-01

327

Rapid adhesive bonding concepts  

NASA Technical Reports Server (NTRS)

Adhesive bonding in the aerospace industry typically utilizes autoclaves or presses which have considerable thermal mass. As a consequence, the rates of heatup and cooldown of the bonded parts are limited and the total time and cost of the bonding process is often relatively high. Many of the adhesives themselves do not inherently require long processing times. Bonding could be performed rapidly if the heat was concentrated in the bond lines or at least in the adherends. Rapid adhesive bonding concepts were developed to utilize induction heating techniques to provide heat directly to the bond line and/or adherends without heating the entire structure, supports, and fixtures of a bonding assembly. Bonding times for specimens are cut by a factor of 10 to 100 compared to standard press bonding. The development of rapid adhesive bonding for lap shear specimens (per ASTM D1003 and D3163), for aerospace panel bonding, and for field repair needs of metallic and advanced fiber reinforced polymeric matrix composite structures are reviewed.

Stein, B. A.; Tyeryar, J. R.; Hodges, W. T.

1984-01-01

328

Adhesion by pathogenic corynebacteria.  

PubMed

Pathogenic members of the genus Corynebacterium cause a wide range of serious infections in humans including diphtheria. Adhesion to host cells is a crucial step during infection. In Corynebacterium diphtheriae, adhesion is mediated primarily by filamentous structures called pili or fimbriae that are covalently attached to the bacterial cell wall. C. diphtheriae produces three distinct pilus structures, SpaA-, SpaD- and SpaH-type pili. Similar to other types, the prototype SpaA pilus consists of SpaA forming the pilus shaft and two minor pilins SpaB and SpaC located at the base and at the tip, respectively. The minor pilins SpaB/SpaC are critical for bacterial binding to human pharyngeal cells, and thus represent the major adhesins of corynebacteria. Like pili of many other gram-positive microbes, the assembly of corynebacterial pili occurs by a two-step mechanism, whereby pilins are covalently polymerized by a transpeptidase enzyme named pilin-specific sortase and the generated pilus polymer is subsequently anchored to the cell wall peptidoglycan via the base pilin by the housekeeping sortase or a non-polymerizing sortase. This chapter reviews the current knowledge of corynebacterial adhesion, with a specific focus on pilus structures, their assembly, and the mechanism of adhesion mediated by pili. PMID:21557059

Rogers, Elizabeth A; Das, Asis; Ton-That, Hung

2011-01-01

329

Adhesion of explosives.  

PubMed

It is of increasing importance to understand how explosive particles adhere to surfaces in order to understand how to remove them for detection in airport or other security settings. In this study, adhesion forces between royal demolition explosive (cyclotrimethylenetrinitramine) (RDX), pentaerythritol tetranitrate (PETN), and trinitrotoluene (TNT) in their crystalline forms and aluminum coupons with three finishes, acrylic melamine (clear coating), polyester acrylic melamine (white coating) automotive finishes, and a green military-grade finish, were measured and modeled. The force measurements were performed using the atomic force microscopy (AFM)-based colloidal probe microscopy (CPM) method. Explosive particles were mounted on AFM cantilevers and repeatedly brought in and out of contact with the surfaces of interest while the required force needed to pull out of contact was recorded. An existing Matlab-based simulator was used to describe the observed adhesion force distributions, with excellent agreement. In these simulations, the measured topographies of the interacting surfaces were considered, although the geometries were approximated. The simulations were performed using a van der Waals force-based adhesion model and a composite effective Hamaker constant. It was determined that certain combinations of roughness on the interacting surfaces led to preferred particle-substrate orientations that produced extreme adhesion forces. PMID:23510004

Chaffee-Cipich, Michelle N; Sturtevant, Bryce D; Beaudoin, Stephen P

2013-06-01

330

Cell Adhesion Force Microscopy  

Microsoft Academic Search

The adhesion forces of cervical carcinoma cells in tissue culture were measured by using the manipulation force microscope, a novel atomic force microscope. The forces were studied as a function of time and temperature for cells cultured on hydrophilic and hydrophobic polystyrene substrates with preadsorbed proteins. The cells attached faster and stronger at 37 degrees C than at 23 degrees

G. Sagvolden; I. Giaever; E. O. Pettersen; J. Feder

1999-01-01

331

High Temperature Adhesive.  

National Technical Information Service (NTIS)

A substrate assembly and method for its preparation, said substrate assembly comprising at least two substrates adhesively bonded with a cured thermosetting polymer being able to withstand a temperature of 200-400 deg C which polymer is derived from a dip...

T. M. Keller C. M. Roland

1992-01-01

332

History of Adhesives  

Microsoft Academic Search

Adhesives are the diplomats of the polymer world. They exist for the purpose of bringing other materials together; their success is measured by the production cost, properties, and permanence of the assembly. Historically, the starches, protein glues, and natural rubber were supplemented or replaced by phenolics and amino resins for plywood and particleboard; synthetic rubbers for construction, textile bonding, and

Irving Skeist; Jerry Miron

1981-01-01

333

Rapid Adhesive Bonding of Composites  

NASA Technical Reports Server (NTRS)

Strong bonds created in less time and with less power than use of conventional bonding methods. Rapid adhesive bonding (RAB) technique for composites uses high-frequency induction heating toroids to quickly heat metallic susceptor impregnated with thermoplastic adhesive or sandwiched between thermoset or thermoplastic adhesive cloths or films. Susceptor steel screen or perforated steel foil.

Stein, B. A.; Tyeryar, J. R.; Fox, R. L.; Sterling, S. Elmo, Jr.; Buckley, J. D.; Inge, Spencer V., Jr.; Burcher, L. G.; Wright, Robert E., Jr.

1986-01-01

334

Adhesion of Topographically Patterned Elastomers  

Microsoft Academic Search

Controlling adhesion is increasingly important in new technologies including MEMS fabrication, soft lithography, and the development of smart adhesives. We investigate the effect of topographical patterns on the adhesion of polymers. Introducing topographical patterns of axisymmetric features, i.e. circular posts, provides a means to accurately control the formation and failure of an interface. We utilize a Johnson, Kendall, and Roberts

Mark Hageman; Andrew Duncan; Alfred Crosby

2004-01-01

335

Recurrent adhesive small bowel obstruction  

Microsoft Academic Search

Adhesive obstruction of the small bowel complicates about 5% of laparotomies; of these, 5–10% have recurrent attacks. The etiology of adhesions is incompletely understood and attempts to prevent their formation are of unproven value. Patients with recurrent acute obstruction that threatens strangulation, or that fails to subside, require laparotomy. If numerous adhesions have to be divided, it is worth considering

Peter F. Jones; Alexander Munro

1985-01-01

336

Coating Reduces Ice Adhesion  

NASA Technical Reports Server (NTRS)

The Shuttle Ice Liberation Coating (SILC) has been developed to reduce the adhesion of ice to surfaces on the space shuttle. SILC, when coated on a surface (foam, metal, epoxy primer, polymer surfaces), will reduce the adhesion of ice by as much as 90 percent as compared to the corresponding uncoated surface. This innovation is a durable coating that can withstand several cycles of ice growth and removal without loss of anti-adhesion properties. SILC is made of a binder composed of varying weight percents of siloxane(s), ethyl alcohol, ethyl sulfate, isopropyl alcohol, and of fine-particle polytetrafluoroethylene (PTFE). The combination of these components produces a coating with significantly improved weathering characteristics over the siloxane system alone. In some cases, the coating will delay ice formation and can reduce the amount of ice formed. SILC is not an ice prevention coating, but the very high water contact angle (greater than 140 ) causes water to readily run off the surface. This coating was designed for use at temperatures near -170 F (-112 C). Ice adhesion tests performed at temperatures from -170 to 20 F (-112 to -7 C) show that SILC is a very effective ice release coating. SILC can be left as applied (opaque) or buffed off until the surface appears clear. Energy dispersive spectroscopy (EDS) and x-ray photoelectron spectroscopy (XPS) data show that the coating is still present after buffing to transparency. This means SILC can be used to prevent ice adhesion even when coating windows or other objects, or items that require transmission of optical light. Car windshields are kept cleaner and SILC effectively mitigates rain and snow under driving conditions.

Smith, Trent; Prince, Michael; DwWeese, Charles; Curtis, Leslie

2008-01-01

337

High-Mobility Group Box-1 Induces Decreased Brain-Derived Neurotrophic Factor-Mediated Neuroprotection in the Diabetic Retina  

PubMed Central

To test the hypothesis that brain-derived neurotrophic factor-(BDNF-) mediated neuroprotection is reduced by high-mobility group box-1 (HMGB1) in diabetic retina, paired vitreous and serum samples from 46 proliferative diabetic retinopathy and 34 nondiabetic patients were assayed for BDNF, HMGB1, soluble receptor for advanced glycation end products (sRAGE), soluble intercellular adhesion molecule-1 (sICAM-1), monocyte chemoattractant protein-1 (MCP-1), and TBARS. We also examined retinas of diabetic and HMGB1 intravitreally injected rats. The effect of the HMGB1 inhibitor glycyrrhizin on diabetes-induced changes in retinal BDNF expressions was studied. Western blot, ELISA, and TBARS assays were used. BDNF was not detected in vitreous samples. BDNF levels were significantly lower in serum samples from diabetic patients compared with nondiabetics, whereas HMGB1, sRAGE, sICAM-1, and TBARS levels were significantly higher in diabetic serum samples. MCP-1 levels did not differ significantly. There was significant inverse correlation between serum levels of BDNF and HMGB1. Diabetes and intravitreal administration of HMGB1 induced significant upregulation of the expression of HMGB1, TBARS, and cleaved caspase-3, whereas the expression of BDNF and synaptophysin was significantly downregulated in rat retinas. Glycyrrhizin significantly attenuated diabetes-induced downregulation of BDNF. Our results suggest that HMGB1-induced downregulation of BDNF might be involved in pathogenesis of diabetic retinal neurodegeneration.

Nawaz, Mohd Imtiaz; Siddiquei, Mohammad Mairaj; Al-Kharashi, Abdullah S.; Kangave, Dustan; Mohammad, Ghulam

2013-01-01

338

Vitamin C prevents endothelial dysfunction induced by acute exercise in patients with intermittent claudication.  

PubMed

In patients with intermittent claudication, exercise is associated with a marked increase in oxidative stress, likely responsible for systemic endothelial perturbation. In 31 claudicant patients, we assessed the effect of vitamin C administration on the acute changes induced by maximal and submaximal exercise in endothelium-dependent, flow-mediated dilation (FMD), and in plasma levels of thiobarbituric acid-reactive substances (TBARS) and soluble intercellular adhesion molecule-1 (sICAM-1). In 16 claudicants, maximal exercise reduced FMD (from 8.5+/-0.9 to 3.7+/-0.8%, P<0.01), and increased plasma levels of TBARS (from 1.93+/-0.06 to 2.22+/-0.1 nmol/ml, P<0.02) and of sICAM-1 (from 282+/-17 to 323+/-19 ng/ml, P<0.01). In eight of these patients, randomized to vitamin C, exercise-induced changes in FMD and biochemistry were abolished. This beneficial effect was not observed in the eight patients randomized to saline. In 15 patients, who walked until the onset of claudication pain (submaximal exercise), and in ten control subjects, who performed maximal exercise, no changes were observed with exercise. Thus, in claudicants, vitamin C prevents the acute, systemic impairment in endothelial function induced by maximal exercise. This finding provides a rationale for trials investigating antioxidant therapy and cardiovascular risk in patients with intermittent claudication. PMID:12417278

Silvestro, Antonio; Scopacasa, Francesco; Oliva, Gabriella; de Cristofaro, Tiziana; Iuliano, Luigi; Brevetti, Gregorio

2002-12-01

339

Hydroxyurea downregulates endothelin-1 gene expression and upregulates ICAM-1 gene expression in cultured human endothelial cells.  

PubMed

The clinical efficacy of oral hydroxyurea (HU) in adults and children with sickle cell anemia (SCA) cannot solely be explained by its ability to enhance fetal hemoglobin (HbF) expression. Since increased adherence of sickle red blood cells to vascular endothelium is a possible contributing factor to vaso-occlusive crisis (VOC), we explored the effect of HU on human endothelial cell (EC) lines (TrHBMEC and EA-hy 926). We demonstrated that HU, in a dose-dependent and reversible manner, significantly decreased (up to three-fold) the release of endothelin-1 (ET-1), a vasoconstrictor peptide through downregulation (up to three-fold) of ET-1 gene expression. This finding is of therapeutic relevance as SCA patients exhibit elevated serum levels of ET-1 during episodes of VOC and levels correlate with disease severity. Unexpectedly, HU upregulated (up to three-fold) the expression of membrane-bound intercellular cell adhesion molecule 1 (mbICAM-1) and its soluble form (sICAM-1) with a parallel increase in ICAM-1 mRNA expression. Although ICAM-1 does not appear to be involved in the sickle cell adhesion to vascular endothelium, it may exacerbate vaso-occlusion by promoting leukocyte adhesion. The HU-induced increase in mbICAM-1 may appear inconsistent with the clinical benefits confered by HU. However, both the increase in sICAM-1- and HU-induced leukocyte reduction in patients, may counteract the potentially detrimental effect of elevated mbICAM-1 expression. Also HU reduces the expression of vascular cell adhesion molecule (VCAM-1) on EC. Since HU reduces the very late antigen 4-positive reticulocytes in SCA patients, a ligand for VCAM-1, HU-induced downregulation of VCAM-1 on EC will very likely decrease the reticulocyte-endothelium adhesion. Thus, HU, apart from inducing HbF expression in the red cell, also affects the expression profile of EC compartment. PMID:12931135

Brun, M; Bourdoulous, S; Couraud, P O; Elion, J; Krishnamoorthy, R; Lapoumeroulie, C

2003-01-01

340

Environmentally compliant adhesive joining technology  

SciTech Connect

Adhesive joining offers one method of assembling products. Advantages of adhesive joining/assembly include distribution of applied forces, lighter weight, appealing appearance, etc. Selecting environmentally safe adhesive materials and accompanying processes is paramount in today`s business climate if a company wants to be environmentally conscious and stay in business. Four areas of adhesive joining (adhesive formulation and selection, surface preparation, adhesive bonding process, waste and pollution generation/cleanup/management) all need to be carefully evaluated before adhesive joining is selected for commercial as well as military products. Designing for six sigma quality must also be addressed in today`s global economy. This requires material suppliers and product manufacturers to work even closer together.

Tira, J.S.

1996-08-01

341

Adhesion barrier reduces postoperative adhesions after cardiac surgery.  

PubMed

Reoperation in cardiac surgery is associated with increased risk due to surgical adhesions. Application of a bioresorbable material could theoretically reduce adhesions and allow later development of a free dissection plane for cardiac reoperation. Twenty-one patients in whom a bioresorbable hyaluronic acid-carboxymethylcellulose adhesion barrier had been applied in a preceding surgery underwent reoperations, while 23 patients underwent reoperations during the same period without a prior adhesion barrier. Blinded observers graded the tenacity of the adhesions from surgical video recordings of the reoperations. No excessive bleeding requiring wound reexploration, mediastinal infection, or other complication attributable to the adhesion barrier occurred. Multiple regression analysis showed that shorter duration of the preceding surgery, non-use of cardiopulmonary bypass in the preceding surgery, and use of the adhesion barrier were significantly associated with less tenacious surgical adhesions. The use of a bioresorbable material in cardiac surgery reduced postoperative adhesions, facilitated reoperation, and did not promote complications. The use of adhesion barrier is recommended in planned staged procedures and those in which future reoperation is likely. PMID:22718712

Kaneko, Yukihiro; Hirata, Yasutaka; Achiwa, Ikuya; Morishita, Hiroyuki; Soto, Hajime; Kobayahsi, Jotaro

2012-06-01

342

Biophysics of Cadherin Adhesion  

PubMed Central

Classical cadherins are the principle adhesive proteins at cohesive intercellular junctions, and are essential proteins for morphogenesis and tissue homeostasis. Because subtype-dependent differences in cadherin adhesion are at the heart of cadherin functions, several structural and biophysical approaches have been used to elucidate relationships between cadherin structures, biophysical properties of cadherin bonds, and cadherin-dependent cell functions. Some experimental approaches appeared to provide conflicting views of the cadherin binding mechanism. However, recent structural and biophysical data, as well as computer simulations generated new insights into classical cadherin binding that increasingly reconcile diverse experimental findings. This review summarizes these recent findings, and highlights both the consistencies and remaining challenges needed to generate a comprehensive model of cadherin interactions that is consistent with all available experimental data.

Leckband, Deborah; Sivasankar, Sanjeevi

2012-01-01

343

Laparoscopic Lysis of Adhesions  

Microsoft Academic Search

Background  Intra-abdominal adhesions constitute between 49% and 74% of the causes of small bowel obstruction. Traditionally, laparotomy\\u000a and open adhesiolysis have been the treatment for patients who have failed conservative measures or when clinical and physiologic\\u000a derangements suggest toxemia and\\/or ischemia. With the increased popularity of laparoscopy, recent promising reports indicate\\u000a the feasibility and potential superiority of the minimally invasive approach

Samuel Szomstein; Emanuele Lo Menzo; Conrad Simpfendorfer; Nathan Zundel; Raul J. Rosenthal

2006-01-01

344

Adhesive bond degradation sensor  

NASA Astrophysics Data System (ADS)

Early detection of adhesive bond degradation using sensing elements embedded within the 100um bond-line of aluminium epoxy adhesive joints has been demonstrated. Sensing elements of varying heights were fabricated at the ends of narrow conductors on a flexi-circuit carrier. This construction simulates the active sensing region on a patented silicon adhesive bond degradation sensor and has been used to characterize the sensing elements without the expense and time associated with fabricating the complete integrated silicon sensor. The highest elements on the flexi-circuit serve both as electrical pickup studs, providing a circuit from the flexi-circuit to the top aluminium plate, and as spacers to ensure that the shorter sensing elements do not contact the aluminium plate. The non-contacting sensing elements are thus arranged to be close to the metal/adhesive interface and are sensitive to any change in conductivity in this region due to release of ions as the interface is degraded by the environment. Accelerated aging tests were performed on flexi-circuit sensors embedded in the bond-line of double cantilever beam specimens. The specimens were immersed in 50° C water and pre-loaded to just initiate a crack. Load on the specimen was then maintained by applying a constant load point displacement with a very low velocity to ensure that the environment would degrade the bond-line in advance of the crack front. The change of load and the conductivity measured by the sensing elements were then logged with time. The onset of bond degradation was detected approximately 10-20 mm ahead of the crack tip.

Wilson, Alan R.; Olsson-Jacques, Christina; Muscat, Richard F.

2002-12-01

345

Polyimide adhesive bonding  

NASA Technical Reports Server (NTRS)

Adhesive systems which could be used to bond composite-to-composite, composite-to-titanium, and honeycomb sandwich structures with operational capability at 589K for a minimum of 125 hours were evaluated. Evaluations were based on mechanical property tests such as lap shear and flatwise tensile and on processability. Quasi-isotropic Celion 6000/PMR-15 composite adherend was used to construct lap shear and flatwise tensile specimens. Hexcel's HRH-327-3/16-6.0 glass polyimide honeycomb core was also utilized in the flatwise tensile specimens. Numerous processing variations were also studied that led to selected cure cycles for each adhesive. Shear specimens having either 12 mm or 75 mm overlaps were used to determine the effect of bond size on processability and lap shear properties. The data indicate that processing of FM-34, FM-34B-18, LARC-13 and NRO56X can be achieved using a cure compatible with the composite adherend. No significant differences in mechanical properties were observed among the three adhesive systems and all three are suitable candidates for 589K/125 hour service.

Progar, D.

1979-01-01

346

Cell adhesion on nanotopography  

NASA Astrophysics Data System (ADS)

Cell adhesion, a key element in understanding the cell-biomaterial interactions, underpins proper cell growth, function and survival. Understanding the parameters influencing cell adhesion is critical for applications in biosensors, implants and bioreactors. A gradient surface is used to study the effect of the surface topography on cell adhesion. A gradient surface is generated by block copolymer and homopolymer blends. The two homopolymers will phase separate on the micron scale and gradually decrease to nano-scale by the microphase separation of the diblock. Gradient surfaces offer a unique opportunity to probe lateral variations in the topography and interactions. Using thin films of mixtures of diblock copolymers of PS-b-MMA with PS and PMMA homopolymers, where the concentration of the PS-b-MMA varies across the surface, a gradient in the size scale of the morphology, from the nanoscopic to microscopic, was produced. By UV exposure, the variation in morphology translated into a variation in topography. The extent of cell spreading and cytoskeleton formation was investigated and marked dependence on the length scale of the surface topography was found.

Tsai, Irene; Kimura, Masahiro; Stockton, Rebecca; Jacobson, Bruce; Russell, Thomas

2003-03-01

347

Development of phosphorylated adhesives  

NASA Technical Reports Server (NTRS)

The synthesis of epoxy prepolymers containing phosphorus was carried out in such a manner as to provide adhesives containing at least 5 percent of this element. The purpose of this was to impart fire retardant properties to the adhesive. The two epoxy derivatives, bis(4-glycidyl-oxyphenyl)phenylphosphine oxide and bis(4-glycidyl-2-methoxyphenyl)phenylphosphonate, and a curing agent, bis(3-aminophenyl)methylphosphine oxide, were used in conjunction with one another and along with conventional epoxy resins and curing agents to bond Tedlar and Polyphenylethersulfone films to Kerimid-glass syntactic foam-filled honeycomb structures. Elevated temperatures are required to cure the epoxy resins with the phosphorus-contaning diamine; however, when Tedlar is being bonded, lower curing temperatures must be used to avoid shrinkage and the concomitant formation of surface defects. Thus, the phosphorus-containing aromatic amine curing agent cannot be used alone, although it is possible to use it in conjunction with an aliphatic amine which would allow lower cure temperatures to be used. The experimental epoxy resins have not provided adhesive bonds quite as strong as those provided by Epon 828 when compared in peel tests, but the differences are not very significant. It should be noted, if optimum properties are to be realized. In any case the fire retardant characteristics of the neat resin systems obtained are quite pronounced, since in most cases the self-extinguishing properties are evident almost instantly when specimens are removed from a flame.

Bilow, N.; Giants, T. W.; Jenkins, R. K.; Campbell, P. L.

1983-01-01

348

Ceramic microstructure and adhesion  

NASA Technical Reports Server (NTRS)

When a ceramic is brought into contact with a ceramic, a polymer, or a metal, strong bond forces can develop between the materials. The bonding forces will depend upon the state of the surfaces, cleanliness and the fundamental properties of the two solids, both surface and bulk. Adhesion between a ceramic and another solid are discussed from a theoretical consideration of the nature of the surfaces and experimentally by relating bond forces to interface resulting from solid state contact. Surface properties of ceramics correlated with adhesion include, orientation, reconstruction and diffusion as well as the chemistry of the surface specie. Where a ceramic is in contact with a metal their interactive chemistry and bond strength is considered. Bulk properties examined include elastic and plastic behavior in the surficial regions, cohesive binding energies, crystal structures and crystallographic orientation. Materials examined with respect to interfacial adhesive interactions include silicon carbide, nickel zinc ferrite, manganese zinc ferrite, and aluminum oxide. The surfaces of the contacting solids are studied both in the atomic or molecularly clean state and in the presence of selected surface contaminants.

Buckley, D. H.

1984-01-01

349

Ceramic microstructure and adhesion  

NASA Technical Reports Server (NTRS)

When a ceramic is brought into contact with a ceramic, a polymer, or a metal, strong bond forces can develop between the materials. The bonding forces will depend upon the state of the surfaces, cleanliness and the fundamental properties of the two solids, both surface and bulk. Adhesion between a ceramic and another solid are discussed from a theoretical consideration of the nature of the surfaces and experimentally by relating bond forces to interface resulting from solid state contact. Surface properties of ceramics correlated with adhesion include, orientation, reconstruction and diffusion as well as the chemistry of the surface specie. Where a ceramic is in contact with a metal their interactive chemistry and bond strength is considered. Bulk properties examined include elastic and plastic behavior in the surficial regions, cohesive binding energies, crystal structures and crystallographic orientation. Materials examined with respect to interfacial adhesive interactions include silicon carbide, nickel zinc ferrite, manganese zinc ferrite, and aluminum oxide. The surfaces of the contacting solids are studied both in the atomic or molecularly clean state and in the presence of selected surface contaminants.

Buckley, D. H.

1985-01-01

350

EVIDENCE OF PROATHEROGENIC INFLAMMATION IN POLYCYSTIC OVARY SYNDROME  

PubMed Central

Women with Polycystic Ovary Syndrome (PCOS) have chronic low level inflammation which can increase the risk of atherogenesis. We measured circulating proatherogenic inflammatory mediators in women with PCOS (8 lean - BMI, 18–25 kg/m2, 8 obese -BMI, 30–40 kg/m2) and weight-matched controls (8 lean, 8 obese). Blood samples were obtained fasting and 2 hours after glucose ingestion to measure interleukin-6 (IL-6), soluble intercellular adhesion molecule-1 (sICAM-1), monocyte chemotactic protein-1 (MCP-1), C-reactive protein (CRP), matrix metalloproteinase-2 (MMP-2), plasminogen activator inhibitor-1 (PAI-1), and activated nuclear factor ?B (NF?B) in mononuclear cells. Truncal fat was determined by DEXA. Fasting MCP-1 levels were elevated in lean women with PCOS compared to lean controls (159.9±14.1 vs. 121.2±5.4 pg/ml, p<0.02). Hyperglycemia failed to suppress MMP-2 in lean women with PCOS compared to lean controls (1.7±1.2 vs. ?4.8±1.6 pg/ml, p<0.002). Among women with PCOS, obese individuals exhibited higher fasting sICAM-1 (16.1±0.8 vs. 10.5±1.0 ng/ml, p<0.03) and PAI-1 (6.1±0.7 vs. 3.4±0.8 ng/ml, p<0.03) levels. Trend analysis revealed higher (p<0.005) IL-6, sICAM-1, CRP and PAI-1, systolic and diastolic blood pressures, triglycerides, fasting insulin and HOMA-IR in women with PCOS compared to weight-matched controls, and the highest levels in the obese regardless of PCOS status. Fasting MCP-1 levels correlated with activated NF?B during hyperglycemia (p<0.05) and androstendione (p<0.004). Truncal fat correlated with fasting IL-6 (p<0.004), sICAM-1 (p<0.006), CRP (p<0.0009) and PAI-1 (p<0.02). We conclude that both PCOS and obesity contribute to a proatherogenic state, but in women with PCOS, abdominal adiposity and hyperandrogenism may exacerbate the risk of atherosclerosis.

Gonzalez, Frank; Rote, Neal S.; Minium, Judi; Kirwan, John P.

2009-01-01

351

Dehydroepiandrosterone administration modulates endothelial and neutrophil adhesion molecule expression in vitro  

PubMed Central

Introduction The steroid hormone dehydroepiandrosterone (DHEA) exerts protecting effects in the treatment of traumatic and septic complications in several animal models. This effect goes along with reduced amounts of infiltrating immune cells in organs such as lung and liver. However, the underlying mechanisms of DHEA action are still not known. Adhesion molecules are important for the extravasation of neutrophils into organs where they may exhibit detrimental effects. Therefore, we investigated the in vitro effect of DHEA on the expression pattern of adhesion molecules of human endothelial cells and neutrophils. Methods Endothelial cells derived from human umbilical cord were subjected to an lipopolysaccharide (LPS) challenge. DHEA was administered in two different concentrations, 10-5 M and 10-8 M, as a single stimulus or in combination with LPS challenge. After two, four and 24 hours, fluorescence activated cell sorter (FACS) analysis for vascular cell adhesion molecule-1, intercellular adhesion molecule-1 and E-selectin was performed. Neutrophils were freshly isolated from blood of 10 male healthy volunteers, stimulated the same way as endothelial cells and analyzed for surface expression of L-selectin, CD11b and CD18. Results In the present study, we were able to demonstrate effects of DHEA on the expression of every adhesion molecule investigated. DHEA exhibits opposite effects to those seen upon LPS exposure. Furthermore, these effects are both time and concentration dependent as most DHEA specific effects could be detected in the physiological concentration of 10-8 M. Conclusion Thus, we conclude that one mechanism by which DHEA may exert its protection in animal models is via the differential regulation of adhesion molecule expression.

Barkhausen, Tanja; Westphal, Britt-Mailin; Putz, Claudia; Krettek, Christian; van Griensven, Martijn

2006-01-01

352

Candida albicans stimulates cytokine production and leukocyte adhesion molecule expression by endothelial cells.  

PubMed Central

Endothelial cells have the potential to influence significantly the host immune response to blood-borne microbial pathogens, such as Candida albicans. We investigated the ability (of this organism to stimulate endothelial cell responses relevant to host defense in vitro. Infection with C. albicans induced endothelial cells to express mRNAs encoding E-selectin, intercellular adhesion molecule 1, vascular cell adhesion molecule 1, interleukin 6, interleukin 8, monocyte chemoattractant protein 1, and inducible cyclooxygenase (cox2). All three leukocyte adhesion molecule proteins were expressed on the surfaces of the endothelial cells after 8 h of exposure to C. albicans. An increase in secretion of all three cytokines was found after 12 h of infection. Cytochalasin D inhibited accumulation of the endothelial cell cytokine and leukocyte adhesion molecule mRNAs in response to C. albicans, suggesting that endothelial cell phagocytosis of the organism is required to induce this response. Live Candida tropicalis, Candida glabrata, a nongerminating strain of C. albicans, and killed C. albicans did not stimulate the expression of any of the cytokine or leukocyte adhesion molecule mRNAs. These findings indicate that a factor associated with live, germinating C. albicans is required for induction of endothelial cell mRNA expression. Furthermore, since endothelial cells phagocytize killed C. albicans, phagocytosis is likely necessary but not sufficient for this organism to stimulate mRNA accumulation. In conclusion, the secretion of proinflammatory cytokines and expression of leukocyte adhesion molecules by endothelial cells in response to C. albicans could enhance the host defense against this organism by contributing to the recruitment of activated leukocytes to sites of intravascular infection.

Filler, S G; Pfunder, A S; Spellberg, B J; Spellberg, J P; Edwards, J E

1996-01-01

353

Dental adhesives of the future.  

PubMed

The current trend in the development of dentin adhesives attempts to simplify bonding steps and make them more user-friendly. However, optimizing speed and efficiency should be accomplished without major tradeoffs in the quality or durability of resin bonds. Although dentin adhesives have improved tremendously over the past decade, postoperative sensitivity, incomplete marginal seal, premature bond degradation, biocompatibility, and compromised bonding to abnormal substrates are still considered potential problems associated with their use. Advances in different scientific disciplines will enrich the pool from which ideas may be drawn in designing future dentin adhesives. It is probably on the molecular level that we will see the greatest expansion of horizons. With the advances in biomimetics, future dentin adhesive monomers may contain domains derived from protein-based, underwater bioadhesives secreted by aquatic animals such as mussels and barnacles, making them less dependent on the surface energy of the bonding substrates as well as less susceptible to hydrolytic degradation. As adhesive joints produced by contemporary adhesives are brittle in nature, future adhesive design may incorporate biomimetic intermediate-strength domains that can undergo stepwise reversible unfolding in response to varying functional stress levels before ultimate catastrophic failure of the adhesive joint occurs. These domains may also re-establish folded configurations on stress relaxation, making the adhesive both strong and tough. Using the concept of controlled release, future adhesives may contain fluorescent biosensors that can detect pH changes around leaking restorations. They may even have the capacity to heal autonomously, in response to microcracks formed by functional stresses within the adhesive joint. The ability to self-diagnose and self-repair will increase the life expectancy of adhesive restorations. Future dentin adhesives may also assume a more instrumental role in therapeutics apart from caries prevention. These features may include the controlled release of noncollagenous proteins to promote remineralization of collagen matrices in sound and caries affected dentin, and growth factors to induce controlled formation of reparative dentin. PMID:12236646

Tay, Franklin R; Pashley, David H

2002-01-01

354

Epigallocatechin 3-gallate inhibits 7-ketocholesterol-induced monocyte-endothelial cell adhesion.  

PubMed

7-Ketocholesterol (7KC) induces monocytic adhesion to endothelial cells, and induces arteriosclerosis while high-density lipoprotein (HDL) inhibits monocytic adhesion to the endothelium. Epigallocatechin 3-gallate (EGCG) was found to have a protective effect against arteriosclerosis. Therefore, the purpose of this study was to examine the possible HDL-like mechanisms of EGCG in endothelial cells by investigating whether EGCG inhibits 7KC-induced monocyte-endothelial cell adhesion by activating HDL-dependent signal transduction pathways. 7KC and/or EGCG were added to human endothelial cells (ISO-HAS), and the adhesion of pro-monocytic U937 cells was examined. The expression of genes associated with HDL effects such as Ca(2+)/calmodulin-dependent kinase II (CaMKKII), liver kinase B (LKD1), PSD-95/Dlg/ZO-1 kinase 1 (PDZK1), phosphatidylinositol 3-kinase (PI3K), intercellular adhesion molecule-1 (ICAM-1), monocyte chemotactic protein-1 (MCP-1), and endothelial nitric oxide synthase (eNOS) was examined by RT-PCR, and ICAM-1 protein expression was evaluated by western blot (WB). Production of reactive oxygen species (ROS) was examined with H2DCFDA. 7KC significantly induced adhesion of U937 cells to human endothelial cells while significantly increasing gene expressions of ICAM-1 and MCP-1 and decreasing eNOS and CaMKKII gene expressions. EGCG inhibited 7KC-induced monocytic adhesion to endothelial cells, and induced expression of eNOS and several genes involved in the CaMKKII pathway. Stimulation of endothelial cells with EGCG produced intracellular ROS, whereas treatment with N-acetylcysteine (NAC) blocked EGCG-induced expression of eNOS and CaMKKII. These results suggest that inhibition of monocyte-endothelial cell adhesion by EGCG is associated with CaMKKII pathway activation by ROS. Inhibition of 7KC-induced monocyte-endothelial cell adhesion induced by EGCG may function similarly to HDL. PMID:23567873

Yamagata, Kazuo; Tanaka, Noriko; Suzuki, Koichi

2013-07-01

355

Rolling and adhesion of human tumor cells on vascular endothelium under physiological flow conditions.  

PubMed Central

We investigated the interaction of different human tumor types with resting and IL-1-activated human umbilical vein endothelial cells under laminar flow conditions using a parallel plate flow chamber. Three tumor cell lines (the HT-29M colon carcinoma, the OVCAR-3 ovarian carcinoma, and the T-47D breast carcinoma) showed limited adhesion to unstimulated endothelial cells at any of the shear stress levels tested, while rolling and massive adhesion of tumor cells were observed on IL-1-activated endothelial cells. Three other tumor cell lines (the A375M and A2058 melanomas and the MG-63 osteosarcoma) did not adhere on resting endothelial cells at high shear stress (> 1.5 dyn/cm2) and started to adhere with decreasing shear stress; the number of adherent cells increased steeply on IL-1-activated endothelial cells, but no cell rolling was observed even at the highest shear stress. These mechanisms of tumor cell interaction with endothelial cells were analyzed in detail using the HT-29M colon carcinoma and the A375M melanoma. Incubation of activated endothelial cells with a monoclonal antibody against E-selectin inhibited rolling and adhesion of HT-29M, but had no effect on the adhesion of A375M cells; monoclonal antibody against vascular cell adhesion molecule-1 reduced the adhesion of A375M cells and had no effect on HT-29M. The selective interaction of these two molecules with tumor cells was confirmed by measuring the adhesion of tumor cells on immobilized soluble proteins. On E-selectin-coated surfaces, HT-29M cells rolled during perfusion experiments without subsequent adhesion, while A375M cells did not adhere. On vascular cell adhesion molecule-1-coated surfaces, HT-29M cells neither adhered nor rolled, while A375M cells adhered massively without rolling. Under flow conditions, therefore, cells from different tumor types interact with the endothelial surface by different mechanisms, depending on adhesion molecules expressed on the tumor and endothelial cell surface. Images

Giavazzi, R; Foppolo, M; Dossi, R; Remuzzi, A

1993-01-01

356

Impairment of selectin-mediated leukocyte adhesion to venular endothelium in spontaneously hypertensive rats.  

PubMed Central

The present study was designed to elucidate whether molecular mechanisms for leukocyte adhesion to microvascular endothelium may differ between spontaneously hypertensive rats and Wistar Kyoto rats. Leukocyte rolling and adhesion were investigated while monitoring venular wall shear rates in the mesenteric microcirculation stimulated with histamine or tert-butyl hydroperoxide in the two strains. In Wistar Kyoto rats, 10 microM histamine as well as 500 microM tertbutyl hydroperoxide promoted a significant reduction of venular leukocyte rolling velocity and subsequent adhesion. These changes in leukocyte behavior were blocked by monoclonal antibodies against P-selectin (PB 1.3) and against sialyl Lewis X-like carbohydrates (2H5). However, spontaneously hypertensive rats exhibited a blunted response of the stimulus-elicited leukocyte rolling, which was associated with impairment of venular P-selectin expression as well as a decrease in the expression of sialyl Lewis X-like carbohydrates on circulating neutrophils. No significant differences were detected between the two strains not only in the surface CD11b/CD18 expression but also in the CD18-mediated adhesivity of neutrophils to intracellular adhesion molecule-1 transfectants in vitro. These results suggest that impairment of selectin-mediated leukocyte adhesion is an event responsible for disorders of inflammatory responses in spontaneously hypertensive rats. Images

Suematsu, M; Suzuki, H; Tamatani, T; Iigou, Y; DeLano, F A; Miyasaka, M; Forrest, M J; Kannagi, R; Zweifach, B W; Ishimura, Y

1995-01-01

357

A standardized bamboo leaf extract inhibits monocyte adhesion to endothelial cells by modulating vascular cell adhesion protein-1  

PubMed Central

Bamboo leaves (Phyllostachys pubescens Mazel ex J. Houz (Poacea)) have a long history of food and medical applications in Asia, including Japan and Korea. They have been used as a traditional medicine for centuries. We investigated the mechanism of anti-inflammatory activity of a bamboo leaf extract (BLE) on tumor necrosis factor-alpha (TNF-?)-induced monocyte adhesion in human umbilical vein endothelial cells (HUVECs). Exposure of HUVECs to BLE did not inhibit cell viability or cause morphological changes at concentrations ranging from 1 µg/ml to 1 mg/ml. Treatment with 0.1 mg/ml BLE caused 63% inhibition of monocyte adhesion in TNF-?-activated HUVECs, which was associated with 38.4% suppression of vascular cell adhesion molecule-1 expression. Furthermore, TNF-?-induced reactive oxygen species generation was decreased to 47.9% in BLE treated TNF-?-activated HUVECs. BLE (0.05 mg/ml) also caused about 50% inhibition of interleukin-6 secretion from lipopolysaccharide-stimulated monocyte. The results indicate that BLE may be clinically useful as an anti-inflammatory or anti-oxidant for human cardiovascular disease including atherosclerosis.

Choi, Sunga; Park, Myoung Soo; Lee, Yu Ran; Lee, Young Chul; Kim, Tae Woo; Do, Seon-Gil; Kim, Dong Seon

2013-01-01

358

[Study of different adhesive systems adhesion to dentine].  

PubMed

The breaking strength of different adhesive systems (AdheSE, Contax, Ecusit Primer Mono and Clearfil Se Bond) was studied on 60 teeth. The most breaking strength was demonstrated by system Clearfil Se Bond--29.434+/-0.350 MPa. The least breaking strength from the studied bondings was demonstrated by the system AdheSe--23.708+/-0.068 MPa. The breaking strength of the adhesive system Clearfil Se Bond was by 21% higher than the corresponding value of the system Contax (24.312+/-0.086 MPa) and by 11% higher than the corresponding value of the system Ecusit (26.504+/-0.143 MPa). PMID:17495807

Maksimovskaia, L N; Kosinova, E Iu

2007-01-01

359

?-Oryzanol reduces adhesion molecule expression in vascular endothelial cells via suppression of nuclear factor-?B activation.  

PubMed

?-Oryzanol (?-ORZ) is a mixture of phytosteryl ferulates purified from rice bran oil. In this study, we examined whether ?-ORZ represents a suppressive effect on the lipopolysaccharide (LPS)-induced adhesion molecule expression on vascular endothelium. Treatment with LPS elevated the mRNA expression of vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and E-selectin in bovine aortic endothelial cells (BAECs). Pretreatment with ?-ORZ dose-dependently decreased the LPS-mediated expression of these genes. Western blotting also revealed that pretreatment with ?-ORZ dose-dependently inhibited LPS-induced VCAM-1 expression in human umbilical vein endothelial cells. Consistently, pretreatment with ?-ORZ dose-dependently reduced LPS-induced U937 monocyte adhesion to BAECs. In immunofluorescence, LPS caused nuclear factor-?B (NF-?B) nuclear translocation in 40% of BAECs, which indicates NF-?B activation. Pretreatment with ?-ORZ, as well as its components (cycloartenyl ferulate, ferulic acid, or cycloartenol), dose-dependently inhibited LPS-mediated NF-?B activation. Collectively, our results suggested that ?-ORZ reduced LPS-mediated adhesion molecule expression through NF-?B inhibition in vascular endothelium. PMID:22401580

Sakai, Satoshi; Murata, Takahisa; Tsubosaka, Yoshiki; Ushio, Hideki; Hori, Masatoshi; Ozaki, Hiroshi

2012-04-01

360

Adhesion properties of gecko setae  

NASA Astrophysics Data System (ADS)

Millions of keratin hairs on gecko feet, called setae, act as a spectacular dry adhesive. Each seta branches into hundreds of smaller fibers that terminate in spatula-shaped ends. Morphological differences between the setae from different gecko species are suspected to affect both single-seta and whole-animal adhesion properties. Single-seta adhesive force measurements made using a MEMS piezoresistive cantilever capable of two-axis measurements are presented.

Hill, Ginel; Peattie, Anne; Daniels, Roxanne; Full, Robert; Kenny, Thomas

2005-03-01

361

Membrane adhesion and domain formation  

Microsoft Academic Search

We review theoretical results for the adhesion-induced phase behavior of biomembranes. The focus is on models in which the membranes are represented as discretized elastic sheets with embedded adhesion molecules. We present several mechanism that lead to the formation of domains during adhesion, and discuss the time-dependent evolution of domain patterns obtained in Monte-Carlo simulations. The simulated pattern dynamics has

Thomas R. Weikl; Reinhard Lipowsky

2007-01-01

362

Analysis and testing of adhesive bonds  

NASA Technical Reports Server (NTRS)

An adhesive fracture mechanics approach is described with reference to the identification and design of the best tests for evaluating a given adhesive, the definition of the most meaningful fundamental parameters by which adhesives might be characterized, and the application of these parameters to the design of joints and to the prediction of their performance. Topics include standard adhesive test techniques, the theory of adhesive fracture, and adhesive fracture energy tests. Analytical methods and computer techniques for adhesive bonding, chemical and physical aspects of adhesive fracture, and specific applications and aspects of adhesive fracture mechanics are discussed.

Anderson, G. P.; Bennett, S. J.; Devries, K. L.

1977-01-01

363

Hot melt adhesive attachment pad  

NASA Technical Reports Server (NTRS)

A hot melt adhesive attachment pad for releasably securing distinct elements together is described which is particularly useful in the construction industry or a spatial vacuum environment. The attachment pad consists primarily of a cloth selectively impregnated with a charge of hot melt adhesive, a thermo-foil heater, and a thermo-cooler. These components are securely mounted in a mounting assembly. In operation, the operator activates the heating cycle transforming the hot melt adhesive to a substantially liquid state, positions the pad against the attachment surface, and activates the cooling cycle solidifying the adhesive and forming a strong, releasable bond.

Fox, R. L.; Frizzill, A. W.; Little, B. D.; Progar, D. J.; Coultrip, R. H.; Couch, R. H.; Gleason, J. R.; Stein, B. A.; Buckley, J. D.; St.clair, T. L. (inventors)

1984-01-01

364

Silane adhesion catalysts  

US Patent & Trademark Office Database

Alkanolamines intentionally incorporated with aminosilanes into surface films have been discovered to provide exceptional levels of adhesive performance when overcoated with any of a variety of paints and polymers. This invention is widely applicable to paints, including polyurethane coatings. It provides bonding to siliceous, polymeric, and other surface types. Practical methods for depositing the needed film from polar solvents are disclosed. Also disclosed is an evaluated general-purpose formulation. This appealing formulation provides cleaning and wetting on a great variety of surfaces and has balanced volatility, low toxicity, low corrosivity, long shelf life, and water miscibility and rinsability.

2000-02-01

365

Zero adhesion system  

NASA Astrophysics Data System (ADS)

This patent discloses a zero adhesion system whereby a protective missile launch pad is held against an Environmental Protection Material (EPM) coated missile skin surface having an intermediary cloth sheet inbetween. The pad comprises a steel sheet having perforated cleats defined therein, which sheet is affixed to the underside of the pad and releasably bears against the intermediary cloth sheet. This arrangement operates such that the protective missile launch pad is freely released from the missile at launch without adhession to the EPM coated missile skin.

Steinmetz, Joseph N., Jr.

1986-07-01

366

Wetting of cork by polymeric adhesives  

Microsoft Academic Search

The cohesion of cork agglomerates is determined by the strength of the adhesive joint established between the polymeric adhesive and the cork particles. The ability of adhesives to form good joints depends, among other factors, on the wetting of cork by the adhesives. The main objective of this research was to study the behaviour of adhesive drops deposited on cork

M. H. Adao; G. M. Cabrita; C. M. Gomes; B. S. Almeida; A. C. Fernandez; J. C. Bordado

1993-01-01

367

Adhesive flip chip bonding on flexible substrates  

Microsoft Academic Search

Flip chip attach provides the highest interconnection density possible, making this technology attractive for use with high density flex substrates. This paper presents three approaches to a flip chip adhesive process based on flexible polyimide and polyester substrates using Au, Ni-Au and Au stud bumps with anisotropic adhesives, isotropic conductive adhesives and nonconductive adhesives. Isotropic conductive adhesives conduct equally in

R. Aschenbrenner; R. Miessner; H. Reichl

1997-01-01

368

Multiple Inflammatory Biomarker Detection in a Prospective Cohort Study: A Cross-Validation between Well-Established Single-Biomarker Techniques and an Electrochemiluminescense-Based Multi-Array Platform  

PubMed Central

Background In terms of time, effort and quality, multiplex technology is an attractive alternative for well-established single-biomarker measurements in clinical studies. However, limited data comparing these methods are available. Methods We measured, in a large ongoing cohort study (n?=?574), by means of both a 4-plex multi-array biomarker assay developed by MesoScaleDiscovery (MSD) and single-biomarker techniques (ELISA or immunoturbidimetric assay), the following biomarkers of low-grade inflammation: C-reactive protein (CRP), serum amyloid A (SAA), soluble intercellular adhesion molecule 1 (sICAM-1) and soluble vascular cell adhesion molecule 1 (sVCAM-1). These measures were realigned by weighted Deming regression and compared across a wide spectrum of subjects’ cardiovascular risk factors by ANOVA. Results Despite that both methods ranked individuals’ levels of biomarkers very similarly (Pearson’s r all?0.755) absolute concentrations of all biomarkers differed significantly between methods. Equations retrieved by the Deming regression enabled proper realignment of the data to overcome these differences, such that intra-class correlation coefficients were then 0.996 (CRP), 0.711 (SAA), 0.895 (sICAM-1) and 0.858 (sVCAM-1). Additionally, individual biomarkers differed across categories of glucose metabolism, weight, metabolic syndrome and smoking status to a similar extent by either method. Conclusions Multiple low-grade inflammatory biomarker data obtained by the 4-plex multi-array platform of MSD or by well-established single-biomarker methods are comparable after proper realignment of differences in absolute concentrations, and are equally associated with cardiovascular risk factors, regardless of such differences. Given its greater efficiency, the MSD platform is a potential tool for the quantification of multiple biomarkers of low-grade inflammation in large ongoing and future clinical studies.

van Bussel, Bas C. T.; Ferreira, Isabel; van de Waarenburg, Marjo P. H.; van Greevenbroek, Marleen M. J.; van der Kallen, Carla J. H.; Henry, Ronald M. A.; Feskens, Edith J. M.; Stehouwer, Coen D. A.; Schalkwijk, Casper G.

2013-01-01

369

Evaluation of cardiovascular biomarkers In HIV-infected patients switching to abacavir or tenofovir based therapy  

PubMed Central

Abstract Background Our objective was to evaluate and compare the effect of abacavir on levels of biomarkers associated with cardiovascular risk. Methods In an open-label randomized trial, HIV-infected patients were randomized 1:1 to switch from zidovudine/lamivudine to abacavir/lamivudine or tenofovir/emtricitabine. In the present analysis, we measured levels of interleukin-6 (IL-6), high-sensitivity C-reactive protein (hs-CRP), soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular adhesion molecule-1 (sVCAM-1), E-selectin, and myeloperoxidase (MPO) at baseline and 4, 12, and 48 weeks after randomization. D-dimer and fasting lipids were measured at baseline and weeks 12 and 48. Levels of biomarkers at all time points and changes from baseline were compared across study arms using Wilcoxon rank sum test. Results Of 40 included patients, 35 completed 48 weeks of randomized therapy and follow up. Levels of E-selectin (P = 0.004) and sVCAM-1 (P = 0.041) increased transiently from baseline to week 4 in the abacavir arm compared with the tenofovir arm, but no long-term increases were detected. We found no significant differences between study arms in the levels or changes in the levels of sICAM-1, MPO, d-dimer, IL-6, or hs-CRP. Levels of total cholesterol and high density lipoprotein (HDL) increased in the abacavir arm relative to the tenofovir arm, but no difference was found in total cholesterol/HDL ratio. Conclusion In patients randomized to abacavir-based HIV-treatment transient increases were seen in the plasma levels of E-selectin and sVCAM-1 compared with treatment with tenofovir, but no difference between study arms was found in other biomarkers associated with endothelial dysfunction, inflammation, or coagulation. The clinical significance of these findings is uncertain. Trial Regestration Clinicaltrials.gov identifier: NCT00647244.

2011-01-01

370

CADM1 Is a Key Receptor Mediating Human Mast Cell Adhesion to Human Lung Fibroblasts and Airway Smooth Muscle Cells  

PubMed Central

Background Mast cells (MCs) play a central role in the development of many diseases including asthma and pulmonary fibrosis. Interactions of human lung mast cells (HLMCs) with human airway smooth muscle cells (HASMCs) are partially dependent on adhesion mediated by cell adhesion molecule-1 (CADM1), but the adhesion mechanism through which HLMCs interact with human lung fibroblasts (HLFs) is not known. CADM1 is expressed as several isoforms (SP4, SP1, SP6) in HLMCs, with SP4 dominant. These isoforms differentially regulate HLMC homotypic adhesion and survival. Objective In this study we have investigated the role of CADM1 isoforms in the adhesion of HLMCs and HMC-1 cells to primary HASMCs and HLFs. Methods CADM1 overexpression or downregulation was achieved using adenoviral delivery of CADM1 short hairpin RNAs or isoform-specific cDNAs respectively. Results Downregulation of CADM1 attenuated both HLMC and HMC-1 adhesion to both primary HASMCs and HLFs. Overexpression of either SP1 or SP4 isoforms did not alter MC adhesion to HASMCs, whereas overexpression of SP4, but not SP1, significantly increased both HMC-1 cell and HLMC adhesion to HLFs. The expression level of CADM1 SP4 strongly predicted the extent of MC adhesion; linear regression indicated that CADM1 accounts for up to 67% and 32% of adhesion to HLFs for HMC-1 cells and HLMCs, respectively. HLFs supported HLMC proliferation and survival through a CADM1-dependent mechanism. With respect to CADM1 counter-receptor expression, HLFs expressed both CADM1 and nectin-3, whereas HASMCs expressed only nectin-3. Conclusion and Clinical Relevance Collectively these data indicate that the CADM1 SP4 isoform is a key receptor mediating human MC adhesion to HASMCs and HLFs. The differential expression of CADM1 counter-receptors on HLFs compared to HASMCs may allow the specific targeting of either HLMC-HLF or HLMC-HASMC interactions in the lung parenchyma and airways.

Moiseeva, Elena P.; Roach, Katy M.; Leyland, Mark L.; Bradding, Peter

2013-01-01

371

Adhesion of Activated Platelets to Endothelial Cells: Evidence for a GPIIbIIIa-dependent Bridging Mechanism and Novel Roles for Endothelial Intercellular Adhesion Molecule 1 (ICAM-1), a v b 3 Integrin, and GPIb a  

Microsoft Academic Search

Summary Although it has been reported that activated platelets can adhere to intact endothelium, the re- ceptors involved have not been fully characterized. Also, it is not clear whether activated plate- lets bind primarily to matrix proteins at sites of endothelial cell denudation or directly to endo- thelial cells. Thus, this study was designed to further clarify the mechanisms of

Thomas Bombeli; Barbara R. Schwartz; John M. Harlan

372

Adhesive substrates for fibronectin.  

PubMed

In order to promote cell attachment, fibronectin must first undergo activation by a suitable substrate. In this study, 52 materials have been surveyed for their ability a) to bind fibronectin, b) to activate the cell-adhesive property of fibronectin, and c) to support the growth of cells. Many plastics, polysaccharides, metals, and ceramics were found to support cell growth as well as the fibronectin-dependent attachment of cells. Several other substrates have been identified that were inactive in promoting either cell attachment or growth. Hydrophobic substrates were found to be active in fibronectin activation, whereas hydrophilic substrates were found to be inactive. Since fibronectin binds to substrata of extremely varied chemical composition, it is clear that the binding of fibronectin to such substrata is nonspecific in nature. Since protein pretreatment of all substrata, except collagen and poly(L-lysine), abolished the physical binding of fibronectin, the binding of fibronectin to artificial substrata is probably ascribable to a nonspecific hydrophobic protein-substratum interaction. In contrast, several lines of evidence indicate that the interaction between fibronectin and collagen displays biological specificity. Poly(hydroxyethylmethacrylate)(poly(HEMA)), which has previously been shown to be nonadhesive for cells, is demonstrated here to be unique in its inability to bind fibronectin. Addition of one part per million of an adhesive polymer to poly(HEMA) permits fibronectin binding to occur. PMID:7320060

Klebe, R J; Bentley, K L; Schoen, R C

1981-12-01

373

Effect of adhesive thickness on adhesively bonded T-joint  

NASA Astrophysics Data System (ADS)

The aim of this work is to analyze the effect of adhesive thickness on tensile strength of adhesively bonded stainless steel T-joint. Specimens were made from SUS 304 Stainless Steel plate and SUS 304 Stainless Steel perforated plate. Four T-joint specimens with different adhesive thicknesses (0.5, 1.0, 1.5 and 2.0 mm) were made. Experiment result shows T-joint specimen with adhesive thickness of 1.0 mm yield highest maximum load. Identical T-joint specimen jointed by spot welding was also tested. Tensile test shows welded T-Joint had eight times higher tensile load than adhesively bonded T-joint. However, in low pressure application such as urea granulator chamber, high tensile strength is not mandatory. This work is useful for designer in fertilizer industry and others who are searching for alternative to spot welding.

Abdullah, A. R.; Afendi, Mohd; Majid, M. S. Abdul

2013-12-01

374

Effect of fibril shape on adhesive properties  

NASA Astrophysics Data System (ADS)

Research into the gecko's adhesive system revealed a unique architecture for adhesives using tiny hairs. By using a stiff material (?-keratin) to create a highly structured adhesive, the gecko's system demonstrates properties not seen in traditional pressure-sensitive adhesives which use a soft, unstructured planar layer. In contrast to pressure sensitive adhesives, the gecko adhesive displays frictional adhesion, in which increased shear force allows it to withstand higher normal loads. Synthetic fibrillar adhesives have been fabricated but not all demonstrate this frictional adhesion property. Here we report the dual-axis force testing of single silicone rubber pillars from synthetic adhesive arrays. We find that the shape of the adhesive pillar dictates whether frictional adhesion or pressure-sensitive behavior is observed. This work suggests that both types of behavior can be achieved with structures much larger than gecko terminal structures. It also indicates that subtle differences in the shape of these pillars can significantly influence their properties.

Soto, Daniel; Hill, Ginel; Parness, Aaron; Esparza, Noé; Cutkosky, Mark; Kenny, Tom

2010-08-01

375

Alternatives to Solvent-Borne Adhesives.  

National Technical Information Service (NTIS)

Rapidly escalating costs of solvent borne adhesives have now given water borne adhesives a significant economic advantage to further advance the environmental and OSHA forces already acting to reduce solvent usage. Water borne adhesive systems based on ch...

W. C. Kania

1980-01-01

376

Adhesive bonding of aircraft structures  

Microsoft Academic Search

Adhesive bonding of aircraft primary structures has been in use for over 50 years and is still in use on current aircraft projects as a direct alternative to riveting. Bonding of stringers to skins for both fuselage and wing construction and of metallic honeycomb to skins for elevators, ailerons, tabs and spoilers are the main uses for adhesives. Details of

A Higgins

2000-01-01

377

Collision of Adhesive Viscoelastic Particles  

Microsoft Academic Search

The collision of convex bodies is considered for small impact velocity, when plastic deformation and fragmentation may be disregarded. In this regime the contact is governed by forces according to viscoelastic deformation and by adhesion. The viscoelastic interaction is described by a modified Hertz law, while for the adhesive interactions, the model by Johnson, Kendall and Roberts (JKR) is adopted.

Nikolai V. Brilliantov; Thorsten Poeschel

2005-01-01

378

Adhesive Development for Military Bridging.  

National Technical Information Service (NTIS)

The objective of this effort was to develop a family of adhesives suited to structural bonding of U.S. Army bridge members. To be joined were: aluminum to aluminum, aluminum to composite, and composite to composite materials. The adhesives should be non-b...

D. I. Basiulis E. Catsiff R. D. Hermansen S. E. Lau W. E. Elias

1988-01-01

379

Adhesion molecules in autoimmune disease  

Microsoft Academic Search

Leukocyte activation, circulation, and localization to inflammatory sites are dependent on adherence to molecules on other cells or to extracellular matrix ligands. Adhesion molecule expression and interactions are probably involved in initiation and propagation of autoimmune diseases. Adhesion molecules pertinent to the development of autoimmunity are the subject of this review. Material in this review was generated by a manual

Robert W. McMurray

1996-01-01

380

Measuring Adhesion And Friction Forces  

NASA Technical Reports Server (NTRS)

Cavendish balance adapted to new purpose. Apparatus developed which measures forces of adhesion and friction between specimens of solid materials in vacuum at temperatures from ambient to 900 degrees C. Intended primarily for use in studying adhesion properties of ceramics and metals, including silicon carbide, aluminum oxide, and iron-base amorphous alloys.

Miyoshi, Kazuhisa

1991-01-01

381

New type LOC adhesive tapes  

Microsoft Academic Search

A new technology of the plastic package is offered in volume production of 16 Mb DRAM. This new package, called the LOC (Lead On Chip) structured package, is characterized by directly bonding the lead frame to the surface of the chip with a adhesive tape. This technology requires some new type packaging materials. Adhesive tape is the key material used

Y. Okugawa; T. Yoshida; T. Suzuki; H. Nakayoshi

1994-01-01

382

Cyanoacrylate Adhesives in Eye Wounds.  

National Technical Information Service (NTIS)

Three main sets of experiments are described in this report: (1) tolerance of cyanocacrylate adhesives in rabbit eyes; (2) in vitro tensile strength of corneal stroma-stroma and sclera-silicone rubber adhesive joints; and (3) sealing corneal and choroidal...

M. F. Refojo

1969-01-01

383

Severe adhesive small bowel obstruction.  

PubMed

Adhesive small bowel obstruction is a frequent cause of hospital admission. Water soluble contrast studies may have diagnostic and therapeutic value and avoid challenging demanding surgical operations, but if bowel ischemia is suspected, prompt surgical intervention is mandatory. A 58-year-old patient was operated for extensive adhesive small bowel obstruction after having had two previous laparotomies for colorectal surgery, and had a complex clinical course with multiple operations and several complications. Different strategies of management have been adopted, including non-operative management with the use of hyperosmolar water soluble contrast medium, multiple surgical procedures, total parenteral nutrition (TPN) support, and finally use of antiadherences icodextrin solution. After 2 years follow-up the patient was doing well without presenting recurrent episodes of adhesive small bowel obstruction. For patients admitted several times for adhesive small bowel obstruction, the relative risk of recurring obstruction increases in relation to the number of prior episodes. Several s