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1

Soluble intercellular adhesion molecule-1 (s-ICAM-1\\/s-CD54) in diffuse large B-cell lymphoma: association with clinical characteristics and outcome  

Microsoft Academic Search

Background: High serum levels of soluble intercellular adhesion molecule-1(s-ICAM-1\\/s-CD54) have been associated with adverse clinical features and poor outcome in chronic lymphocytic leukemia, Hodgkin's disease and non-Hodgkin's lymphoma, but their value in the different subtypes of non-Hodgkin's lymphoma has not been well addressed. Patients and methods: Our aim was to study the serum levels of s-ICAM-1 in diffuse large B-cell

M. J. Terol; M. Tormo; J. A. Martinez-Climent; I. Marugan; I. Benet; A. Ferrandez; A. Teruel; R. Ferrer; J. García-Conde

2003-01-01

2

Tumour-derived interleukin 1alpha (IL-1alpha) up-regulates the release of soluble intercellular adhesion molecule-1 (sICAM-1) by endothelial cells.  

PubMed Central

Levels of circulating soluble intercellular adhesion molecule-1 (sICAM-1) are elevated in patients affected by solid malignancies; however, the cellular sources generating high levels of sICAM-1 remain to be characterized. Using conditioned media (CM) from seven ICAM-1-positive or -negative neoplastic cells, we demonstrate that tumour-derived interleukin 1alpha (IL-1alpha) significantly (P < 0.05) up-regulates the release of sICAM-1 by human umbilical vein endothelial cells. The intensity of the effect correlated with the amounts of IL-1alpha detectable in CM. Levels of ICAM-1 mRNA were also up-regulated by tumour-secreted IL-1alpha. The up-regulation of the shedding of sICAM-1 and of its expression at protein and mRNA level were completely reversed by the addition of anti-IL-1alpha neutralizing antibodies. Consistent with the in vitro data, tumour endothelia were strongly stained for ICAM-1 compared with autologous normal tissue endothelia. Taken altogether, our observations reveal an IL-1alpha-mediated tumour-endothelium relationship sustaining the shedding of sICAM-1 by endothelial cells. This is a general phenomenon in solid malignancies that correlates with the ability of neoplastic cells to secrete IL-1alpha rather than with their expression of ICAM-1 and/or histological origin. sICAM-1 has been previously shown to inhibit LFA-1/ICAM-1-mediated cell-cell interactions; therefore, the ability of neoplastic cells to secrete IL-1alpha is likely to represent a mechanism for their escape from immune interaction. Images Figure 5 Figure 6

Fonsatti, E.; Altomonte, M.; Coral, S.; Cattarossi, I.; Nicotra, M. R.; Gasparollo, A.; Natali, P. G.; Maio, M.

1997-01-01

3

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

4

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

5

Increased plasma concentrations of intercellular adhesion molecule-1 after strenuous exercise associated with muscle damage  

Microsoft Academic Search

.   Intercellular adhesion molecule-1 (ICAM-1) plays an important role in leukocyte migration from the circulation and intervention\\u000a at sites of inflammation. We investigated the effects of various types of exercise on circulating levels of soluble ICAM-1\\u000a (sICAM-1) in normal healthy male adults. Plasma concentrations of sICAM-1 were measured before and after bicycle ergometer\\u000a exercise at intensity of 80% maximal oxygen

Takayuki Akimoto; Masahiro Furudate; Makoto Saitoh; Koichi Sugiura; Takahiro Waku; Takao Akama; Ichiro Kono

2002-01-01

6

Predictive Value of Soluble Intercellular Adhesion Molecule1 for Risk of Ischemic Events in Individuals with Cerebrovascular Disease  

Microsoft Academic Search

Background and Purpose: Cellular adhesion molecules may play a critical role in the inflammatory process leading to atherosclerosis. The purpose of this study was to determine whether soluble intercellular adhesion molecule-1 (sICAM-1) is a predictor of future ischemic events in high-risk individuals and also whether it is associated with carotid artery stenosis. Methods: We conducted a prospective study of sICAM-1

Eric Ehrensperger; Jeffrey Minuk; Liam Durcan; Ariane Mackey; Christina Wolfson; Anne-Marie Fontaine; Robert Côté

2005-01-01

7

Soluble intercellular adhesion molecule-1 and clinical outcomes in patients with acute lung injury  

PubMed Central

Objective To determine if levels of soluble intercellular adhesion molecule-1 (sICAM-1), a marker of alveolar epithelial and endothelial injury, differ in patients with hydrostatic pulmonary edema and acute lung injury (ALI) and are associated with clinical outcomes in patients with ALI. Design, setting, and participants Measurement of sICAM-1 levels in (1) plasma and edema fluid from 67 patients with either hydrostatic pulmonary edema or ALI enrolled in an observational, prospective single center study, and (2) in plasma from 778 patients with ALI enrolled in a large multi-center randomized controlled trial of ventilator strategy. Results In the single-center study, levels of sICAM-1 were significantly higher in both edema fluid and plasma (median 938 and 545 ng/ml, respectively) from ALI patients compared to hydrostatic edema patients (median 384 and 177 ng/ml, P < 0.03 for both comparisons). In the multi-center study, higher plasma sICAM-1 levels were associated with poor clinical outcomes in both unadjusted and multivariable models. Subjects with ALI whose plasma sICAM-1 levels increased over the first 3 days of the study had a higher risk of death, after adjusting for other important predictors of outcome (odds ratio 1.48; 95% CI 1.03–2.12, P = 0.03). Conclusions Both plasma and edema fluid levels of sICAM-1 are higher in patients with ALI than in patients with hydrostatic pulmonary edema. Higher plasma sICAM-1 levels and increasing sICAM-1 levels over time are associated with poor clinical outcomes in ALI. Measurement of sICAM-1 levels may be useful for identifying patients at highest risk of poor outcomes from ALI.

Eisner, Mark D.; Parsons, Polly E.; Thompson, B. Taylor; Conner, Edward R.; Matthay, Michael A.; Ware, Lorraine B.

2009-01-01

8

Prognostic value of plasma soluble intercellular adhesion molecule-1 and endothelin-1 concentration in patients with chronic congestive heart failure  

Microsoft Academic Search

We tested the hypothesis that plasma endothelin-1 (ET-1) and soluble intercellular adhesion molecule-1 (sICAM-1) in patients with congestive heart failure (CHF) are related to subsequent survival, and assessed whether the measurements of these substances provide additional prognostic information to that obtained from clinical and biochemical variables previously known to be associated with high mortality. Plasma levels of sICAM-1 and ET-1

Takayoshi Tsutamoto; Tomoko Hisanaga; Daisuke Fukai; Atsuyuki Wada; Yukiharu Maeda; Keiko Maeda; Masahiko Kinoshita

1995-01-01

9

Increased plasma concentrations of intercellular adhesion molecule-1 after strenuous exercise associated with muscle damage.  

PubMed

Intercellular adhesion molecule-1 (ICAM-1) plays an important role in leukocyte migration from the circulation and intervention at sites of inflammation. We investigated the effects of various types of exercise on circulating levels of soluble ICAM-1 (sICAM-1) in normal healthy male adults. Plasma concentrations of sICAM-1 were measured before and after bicycle ergometer exercise at intensity of 80% maximal oxygen consumption (VO2mag) (16 min), 42 km endurance running and 30-min downhill running at intensity of ventilation threshold (VT). The plasma sICAM-1 level increased 1 day after the endurance running (12%) and downhill running (14%), but not after ergometer exercise. Plasma C-reactive protein (CRP) and creatine kinase (CK) concentrations also increased 1 day after running. Our data suggest that exercise associated with muscle damage and/or inflammation results in increased levels of plasma sICAM-1. The physiological significance of post-exercise high plasma sICAM-1 levels is not clear at this stage, but changes in plasma sICAM-1 may reflect the status of the immune system. PMID:11990724

Akimoto, Takayuki; Furudate, Masahiro; Saitoh, Makoto; Sugiura, Koichi; Waku, Takahiro; Akama, Takao; Kono, Ichiro

2002-01-01

10

High soluble vascular cell adhesion molecule-1 concentrations predict long-term mortality in hemodialysis patients.  

PubMed

PURPOSE: Soluble vascular cell adhesion molecule-1 (sVCAM-1) has a strong association with cardiovascular deaths in patients with coronary artery disease. The aim of this study is to explore the association between sVCAM-1 and cardiovascular mortality in maintenance hemodialysis (MHD) patients. METHODS: Eighty-three clinically stable MHD patients (mean age of 59.4 ± 13.7 years) at a single hospital-based dialysis facility were included. sVCAM-1, soluble intercellular adhesion molecule-1 (sICAM-1), and soluble E-selectin (sE-selectin) were determined at study baseline. The study cohort was divided into higher and lower concentration groups by the median value. The all-cause and cardiovascular mortality of this cohort were followed for 7 years. RESULTS: The mean concentrations of sVCAM-1, sICAM-1, and sE-selectin were 1,393.08 ± 300.96, 230.16 ± 84.86, and 60.01 ± 42.00 ng/mL, respectively. The higher concentration groups of sVCAM-1 and sICAM-1 had higher all-cause mortality by Kaplan-Meier analysis (p = 0.002 and p = 0.030, respectively). Higher sVCAM-1 concentrations had a higher risk of all-cause and cardiovascular mortality (p = 0.006 p = 0.046, respectively) in Cox proportional hazards model analysis. CONCLUSION: In MHD patients, higher sVCAM-1 concentrations independently predict all-cause and cardiovascular mortality. This biomarker may be used as a valid surrogate marker for predicting outcomes. PMID:23563803

Chang, Jia-Feng; Hsu, Shih-Ping; Pai, Mei-Fen; Yang, Ju-Yeh; Chen, Hung-Yuan; Wu, Hon-Yen; Peng, Yu-Sen

2013-04-01

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

Vascular endothelial growth factor and soluble intercellular adhesion molecule-1 in lung adenocarcinoma with malignant pleural effusion: correlations with patient survival and pleural effusion control.  

PubMed

The mechanisms by which vascular endothelial growth factor (VEGF) and soluble intercellular adhesion molecule-1 (sICAM-1) contribute to lung cancer growth have not been fully elucidated. This study aimed to assess the role of VEGF and sICAM-1 in control of pleural effusions (PE) and survival in patients with primary human lung adenocarcinoma. Using enzyme-linked immunoadsorbent assay, the concentrations of VEGF and sICAM-1 were measured in pleural effusions and serum from a total of 79 lung adenocarcinoma patients with malignant pleural effusions (MPE) and 24 patients with tuberculosis. Data were correlated with the efficacy of MPE control and survival. Compared to patients with tuberculosis, the levels of VEGF and sICAM-1 in both PE and serum were significantly higher in patients with lung adenocarcinoma. Statistically significant correlation was observed between PE VEGF levels and MPE control. PE VEGF?2760 pg/ml was used as a cut-off point for failure to MPE control (odds ratio=7.06; 95% confidence interval (CI), 2.40-20.78; P<0.001). The median progression-free survival (PFS) from response assessment was 3 months. In a multivariate analysis, PE VEGF (hazard ratio [HR], 1.16; 95% CI, 1.02-1.32), serum sICAM-1 (HR, 1.90; 95% CI, 1.17-3.07) were confirmed as independent prognostic factors for PFS. The levels of VEGF in PE can be used to predict the therapeutic efficacy in the control of MPE and this, together with serum level of sICAM-1 is potential survival factors in lung adenocarcinoma patients with MPE. PMID:22489699

Qian, Q; Zhan, P; Sun, W K; Zhang, Y; Song, Y; Yu, L K

2012-01-01

13

Soluble interleukin-2 receptor, intercellular adhesion molecule-1 and interleukin-10 serum levels in patients withelanoma  

PubMed Central

Serum soluble interleukin-2 receptor (sIL-2R), intercellular adhesion molecule-1 (sICAM-1) and interleukin-10 (IL-10) have each been reported as useful markers for melanoma progression. To evaluate the clinical relevance of these three markers, we simultaneously analysed their serum levels in patients with melanoma. A longitudinal study with a 3-year follow-up was performed and different stages of the disease were considered. Mean values of sIL-2R were significantly higher than in normal controls in all stages and correlated with the disease progression. The prognosis of patients with levels > 529 U/ml of sIL-2R was significantly poorer than in patients with sIL-2R levels < 529 U/ml. Levels of sICAM-1 were also elevated in melanoma patients, specially at the time of the metastatic disease. Serum IL-10 levels were more frequently detectable in the patients that developed metastasis during follow-up, and the prognosis of patients with detectable IL-10 levels was significantly poorer than in those patients with IL-10 undetected levels. Statistical analysis based on Logistic and Cox regression models showed that only sex, stage and sIL-2R value are factors significantly associated with metastatic progression. Moreover, high levels of sIL-2R could be a risk factor for malignant progression in melanoma. © 2000 Cancer Research Campaign

Boyano, M D; Garcia-Vazquez, M D; Lopez-Michelena, T; Gardeazabal, J; Bilbao, J; Canavate, M L; Galdeano, A Garcia De; Izu, R; Diaz-Ramon, L; Raton, J A; Diaz-Perez, J L

2000-01-01

14

sTNFR-II and sICAM-1 are associated with acute disease and hepatic inflammation in schistosomiasis japonica  

PubMed Central

Soluble intracellular adhesive molecule 1 (sICAM-1) and tumour necrosis factor receptors I (TNFR-1) and II (TNFR-II) have been shown to be associated with numerous liver disorders. Shedding of these membrane proteins can be triggered by the Th1 cytokines, TNF-alpha and IFN-gamma, which are associated with susceptibility or resistance to hepatic schistosomiasis, respectively. Further, TNF-alpha receptors and sICAM-1 have been implicated in periportal fibrosis in advanced human schistosomiasis mansoni and correlate with schistosome granuloma formation in the murine model. We measured serum levels of sICAM-1, TNFR-I and TNFR-II in Chinese patients with different clinically defined stages of schistosomiasis japonica and controls; these included 35 patients with acute schistosomiasis, 45 patients with chronic schistosome infections, 34 advanced patients with evidence of severe morbidity and 20 patients with no known history of exposure to infection. Markedly elevated levels of soluble TNFRs (sTNFRs) and sICAM-1 were observed in the acute and advanced patients compared with the chronic and control groups. Mean sTNFR-II levels were significantly higher in acute patients compared with advanced (P < 0.00001) and chronic patients (P < 0.00001) and showed the strongest association of the markers with acute disease (odds ratio (OR) = 1.099). sTNFR-II and sICAM-1 levels both correlated with infection intensity and there were significant positive correlations observed between eosinophil count and infection intensity (P = 0.0072) and sICAM-1 (P = 0.0014). Although there were significantly higher levels of antigen-specific IgG4 and total IgG in infected individuals compared with controls, none correlated with infection intensity. Further, no differences in IgG4 and total IgG levels were observed between the acute and chronic groups. The results suggest sTNFRs and sICAM-1 are associated with liver inflammation and disease progression. Measurement of sTNFR-II and sICAM-1 levels in serum could serve as additional markers for the diagnosis of acute stage disease and the monitoring of hepatic inflammation in human schistosomiasis japonica.

Ellis, Magda K.; Li, Yuesheng; Hou, Xunya; Chen, Honggen; McManus, Donald P.

2008-01-01

15

Competition between intercellular adhesion molecule-1 and a small-molecule antagonist for a common binding site on the ?l subunit of lymphocyte function-associated antigen-1  

PubMed Central

The lymphocyte function-associated antigen-1 (LFA-1) binding of a unique class of small-molecule antagonists as represented by compound 3 was analyzed in comparison to that of soluble intercellular adhesion molecule-1 (sICAM-1) and A-286982, which respectively define direct and allosteric competitive binding sites within LFA-1’s inserted (I) domain. All three molecules antagonized LFA-1 binding to ICAM-1-Immunoglobulin G fusion (ICAM-1-Ig) in a competition ELISA, but only compound 3 and sICAM-1 inhibited the binding of a fluorescein-labeled analog of compound 3 to LFA-1. Compound 3 and sICAM-1 displayed classical direct competitive binding behavior with ICAM-1. Their antagonism of LFA-1 was surmountable by both ICAM-1-Ig and a fluorescein-labeled compound 3 analog. The competition of both sICAM-1 and compound 3 with ICAM-1-Ig for LFA-1 resulted in equivalent and linear Schild plots with slopes of 1.24 and 1.26, respectively. Cross-linking studies with a photoactivated analog of compound 3 localized the high-affinity small-molecule binding site to the N-terminal 507 amino acid segment of the ? chain of LFA-1, a region that includes the I domain. In addition, cells transfected with a variant of LFA-1 lacking this I domain showed no significant binding of a fluorescein-labeled analog of compound 3 or ICAM-1-Ig. These results demonstrate that compound 3 inhibits the LFA-1/ICAM-1 binding interaction in a directly competitive manner by binding to a high-affinity site on LFA-1. This binding site overlaps with the ICAM-1 binding site on the ? subunit of LFA-1, which has previously been localized to the I domain.

Keating, Susan M.; Clark, Kevin R.; Stefanich, Lisa D.; Arellano, Fred; Edwards, Caroline P.; Bodary, Sarah C.; Spencer, Steven A.; Gadek, Thomas R.; Marsters, James C.; Beresini, Maureen H.

2006-01-01

16

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

17

A Comparative Study of Serum Level of Vascular Cell Adhesion Molecule-1 (sVCAM-1), Intercellular Adhesion Molecule-1(ICAM-1) and High Sensitive C - reactive protein (hs-CRP) in Normal and Pre-eclamptic Pregnancies  

PubMed Central

Objective(s): Pre-eclampsia is characterized by hypertension, dyslipidemia, and increased systemic inflammatory response and has been associated with an increased maternal risk of cardiovascular disease later in life. Endothelial dysfunction is thought to be a central pathogenic feature in pre-eclampsia on the basis of elevated adhesion molecules. The aim of this study was to determine the level of plasma serum level of vascular cell adhesion molecule-1 (sVCAM-1), intercellular adhesion molecule-1(ICAM-1), high sensitive C- reactive protein (hs-CRP) in pre-eclampsia and to compare hs-CRP levels between normal pregnant women, mild and severe pre-eclampsia. Materials and Methods : A cross-sectional study was conducted to determine the plasma concentrations of sVCAM-1, ICAM-1 and hs-CRP in peripheral blood obtained from normal pregnant women (n=40), mild pre-eclampsia (n=37) and severe pre-eclampsia (n=38). Concentrations of soluble adhesion molecule was determined with enzyme linked immunosorbent assay (ELISA). Results: There were significant difference in the means serum hs-CRP between normal pregnant women and mild pre-eclamptic women (P<0.05). Serum concentration of hs-CRP, sVCAM-1(ng.ml) and sICAM-1(ng.ml) were significantly higher in severe pre-eclampsia (P<0.05) than normal pregnancy. There were also significant differences in hs-CRP, s ICAM- 1 and in sVCAM- 1 levels between mild and severe pre-eclampsia (P<0.05). There was no difference in the mean plasma log sVCAM-1, sICAM-1 between normal pregnant women and mild pre-eclamptic women. Conclusion: We have determined the serum concentration of soluble adhesion molecule ICAM-1, VCAM-1 and hsCRP in normal pregnancy and pre-eclampsia. Adhesion molecule is elevated in severe pre-eclampsia compared with normal pregnancy, hsCRP are elevated in severe preeclampsia compared with mild preeclampsia and normal pregnancy and may be useful in predicting the severity of pre-eclampsia.

Farzadnia, Mehdi; Ayatollahi, Hossein; Hasan-zade, Maliheh; Rahimi, Hamid Reza

2013-01-01

18

A Comparative Study of Serum Level of Vascular Cell Adhesion Molecule-1 (sVCAM-1), Intercellular Adhesion Molecule-1(ICAM-1) and High Sensitive C - reactive protein (hs-CRP) in Normal and Pre-eclamptic Pregnancies.  

PubMed

Objective(s): Pre-eclampsia is characterized by hypertension, dyslipidemia, and increased systemic inflammatory response and has been associated with an increased maternal risk of cardiovascular disease later in life. Endothelial dysfunction is thought to be a central pathogenic feature in pre-eclampsia on the basis of elevated adhesion molecules. The aim of this study was to determine the level of plasma serum level of vascular cell adhesion molecule-1 (sVCAM-1), intercellular adhesion molecule-1(ICAM-1), high sensitive C- reactive protein (hs-CRP) in pre-eclampsia and to compare hs-CRP levels between normal pregnant women, mild and severe pre-eclampsia. Materials and Methods : A cross-sectional study was conducted to determine the plasma concentrations of sVCAM-1, ICAM-1 and hs-CRP in peripheral blood obtained from normal pregnant women (n=40), mild pre-eclampsia (n=37) and severe pre-eclampsia (n=38). Concentrations of soluble adhesion molecule was determined with enzyme linked immunosorbent assay (ELISA). Results: There were significant difference in the means serum hs-CRP between normal pregnant women and mild pre-eclamptic women (P<0.05). Serum concentration of hs-CRP, sVCAM-1(ng.ml) and sICAM-1(ng.ml) were significantly higher in severe pre-eclampsia (P<0.05) than normal pregnancy. There were also significant differences in hs-CRP, s ICAM- 1 and in sVCAM- 1 levels between mild and severe pre-eclampsia (P<0.05). There was no difference in the mean plasma log sVCAM-1, sICAM-1 between normal pregnant women and mild pre-eclamptic women. Conclusion: We have determined the serum concentration of soluble adhesion molecule ICAM-1, VCAM-1 and hsCRP in normal pregnancy and pre-eclampsia. Adhesion molecule is elevated in severe pre-eclampsia compared with normal pregnancy, hsCRP are elevated in severe preeclampsia compared with mild preeclampsia and normal pregnancy and may be useful in predicting the severity of pre-eclampsia. PMID:23826490

Farzadnia, Mehdi; Ayatollahi, Hossein; Hasan-Zade, Maliheh; Rahimi, Hamid Reza

2013-05-01

19

The Expression of Endothelial Leukocyte Adhesion Molecule1 (ELAM1), Intercellular Adhesion Molecule1 (ICAM-1), and Vascular Cell Adhesion Molecule1 (VCAM-1) in Experimental Cutaneous Inflammation: A Comparison of Ultraviolet B erythema and Delayed Hypersensitivity  

Microsoft Academic Search

Endothelial cell adhesion molecule-I (ELAM-i), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) are cytokine-regulated cell surface molecules involved in leukocyte adhesion. We have studied two forms of cutaneous inflammation to investigate in vivo the kinetics of adhesion molecule expression in relation to tissue accumulation of leukocytes. Immunohistology was performed on skin biopsies taken from human volunteers at

Paul Norris; Robin N. Poston; D. Sian Thomas; Martin Thornhill; John Hawk; Dorian O. Haskard

1991-01-01

20

Nitric Oxide Mediates the Effect of Fluvastatin on Intercellular Adhesion Molecule1 and Platelet EndothelialCell Adhesion Molecule1 Expressionon Human Endothelial cells  

Microsoft Academic Search

Leukocyte and platelet adhesion to endothelial cells, an early step in the pathogenesis of atherosclerosis, is mediated through adhesion molecules. It has been shown that statins decrease adhesion molecule expression. We examined the hypothesis that fluvastatin decreased intercellular adhesion molecule-1 (ICAM-1) and platelet endothelial cell adhesion molecule-1 (PECAM-1) expression through a nitric oxide-mediated pathway. Human iliac artery endothelial cells were

Eleftherios S. Xenos; Scott L. Stevens; Michael B. Freeman; David C. Cassada; Mitchell H. Goldman

2005-01-01

21

Adhesion Between Human Neutrophils and Immobilized Endothelial Ligand Vascular Cell Adhesion Molecule 1: Divalent Ion Effects  

PubMed Central

Abstract Integrin-mediated adhesion of circulating neutrophils to endothelium during inflammation involves multiple adhesion molecules on both neutrophils and endothelium. Most studies of neutrophil adhesion have focused on adhesion to ICAM-1 (mediated by ?2 integrins), but interaction with the endothelial ligand vascular cell adhesion molecule 1 (VCAM-1) may also play a role in neutrophil adhesion to activated endothelium. In this study we demonstrate significant adhesion between neutrophils and VCAM-1 mediated by ?1 integrins, principally via ?4?1 (VLA-4). We characterize the dynamics of adhesion in terms of rate constants for a two-step bond formation process, the first involving juxtaposition of active molecules with substrate and the second involving bond formation. The results indicate that the first step is rate limiting for VLA-4-VCAM-1 interactions. Changing divalent cation composition affects these coefficients, implicating molecular conformational changes as a key step in the process.

Lomakina, Elena B.; Waugh, Richard E.

2009-01-01

22

Adhesion between human neutrophils and immobilized endothelial ligand vascular cell adhesion molecule 1: divalent ion effects.  

PubMed

Integrin-mediated adhesion of circulating neutrophils to endothelium during inflammation involves multiple adhesion molecules on both neutrophils and endothelium. Most studies of neutrophil adhesion have focused on adhesion to ICAM-1 (mediated by beta(2) integrins), but interaction with the endothelial ligand vascular cell adhesion molecule 1 (VCAM-1) may also play a role in neutrophil adhesion to activated endothelium. In this study we demonstrate significant adhesion between neutrophils and VCAM-1 mediated by beta(1) integrins, principally via alpha(4)beta(1) (VLA-4). We characterize the dynamics of adhesion in terms of rate constants for a two-step bond formation process, the first involving juxtaposition of active molecules with substrate and the second involving bond formation. The results indicate that the first step is rate limiting for VLA-4-VCAM-1 interactions. Changing divalent cation composition affects these coefficients, implicating molecular conformational changes as a key step in the process. PMID:19134480

Lomakina, Elena B; Waugh, Richard E

2009-01-01

23

Elevated pretreatment serum levels of soluble vascular cell adhesion molecule 1 and lactate dehydrogenase as predictors of survival in cutaneous metastatic malignant melanoma.  

PubMed Central

Very rapid progression of disease with a median survival of 6-9 months is a common feature of metastatic cutaneous malignant melanoma. Nevertheless, substantial variability of survival suggests that metastatic cutaneous malignant melanoma can be divided into several biological subgroups. Pretreatment serum levels of soluble adhesion molecules and various clinical parameters in cutaneous metastatic malignant melanoma were evaluated to determine their prognostic value. In this study pretreatment serum levels of soluble vascular cell adhesion molecule 1 (sVCAM-1), soluble intercellular cell adhesion molecule 1 (sICAM-1), soluble endothelial leukocyte adhesion molecule 1 (sE-selectin) and multiple clinical factors were assessed in relation to overall survival of 97 consecutive patients with metastatic cutaneous malignant melanoma seen at our institution between May 1990 and April 1996. For statistical analysis, both univariate and multivariate Cox proportional-hazards models were used. Elevated pretreatment serum levels of sVCAM-1 (P < 0.005) and of lactate dehydrogenase (P < 0.002) were rendered statistically independent and were significantly associated with unfavourable outcome. Patients were assigned to one of three risk categories (low, intermediate and high) according to a cumulative risk score defined as the function of the sum of these two variables. There were significant differences in overall survival (P < 0.0001) between low- (n = 53, 5-year survival probability of 23.3%), intermediate- (n = 29, 5-year survival probability of 9.9%) and high-risk (n = 15) patients. Elevated pretreatment serum levels of sVCAM-1 and of lactate dehydrogenase correlate with poor outcome in metastatic cutaneous malignant melanoma. These data support risk stratification for future therapeutic trials and identify factors that need to be validated in prospective studies and may potentially influence decision-making in palliative management of patients with disseminated cutaneous malignant melanoma.

Franzke, A.; Probst-Kepper, M.; Buer, J.; Duensing, S.; Hoffmann, R.; Wittke, F.; Volkenandt, M.; Ganser, A.; Atzpodien, J.

1998-01-01

24

Glucocorticoid-induced tumor necrosis factor receptor family-related ligand triggering upregulates vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 and promotes leukocyte adhesion.  

PubMed

The interaction of glucocorticoid-induced tumor necrosis factor receptor-family related (GITR) protein with its ligand (GITRL) modulates different functions, including immune/inflammatory response. These effects are consequent to intracellular signals activated by both GITR and GITRL. Previous results have suggested that lack of GITR expression in GITR(-/-) mice decreases the number of leukocytes within inflamed tissues. We performed experiments to analyze whether the GITRL/GITR system modulates leukocyte adhesion and extravasation. For that purpose, we first evaluated the capability of murine splenocytes to adhere to endothelial cells (EC). Our results indicated that adhesion of GITR(-/-) splenocytes to EC was reduced as compared with wild-type cells, suggesting that GITR plays a role in adhesion and that this effect may be due to GITRL-GITR interaction. Moreover, adhesion was increased when EC were pretreated with an agonist GITR-Fc fusion protein, thus indicating that triggering of GITRL plays a role in adhesion by EC regulation. In a human in vitro model, the adhesion to human EC of HL-60 cells differentiated toward the monocytic lineage was increased by EC pretreatment with agonist GITR-Fc. Conversely, antagonistic anti-GITR and anti-GITRL Ab decreased adhesion, thus further indicating that GITRL triggering increases the EC capability to support leukocyte adhesion. EC treatment with GITR-Fc favored extravasation, as demonstrated by a transmigration assay. Notably, GITRL triggering increased intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression and anti-ICAM-1 and anti-VCAM-1 Abs reversed GITR-Fc effects. Our study demonstrates that GITRL triggering in EC increases leukocyte adhesion and transmigration, suggesting new anti-inflammatory therapeutic approaches based on inhibition of GITRL-GITR interaction. PMID:23892569

Lacal, Pedro Miguel; Petrillo, Maria Grazia; Ruffini, Federica; Muzi, Alessia; Bianchini, Rodolfo; Ronchetti, Simona; Migliorati, Graziella; Riccardi, Carlo; Graziani, Grazia; Nocentini, Giuseppe

2013-07-26

25

Detection of circulating intercellular adhesion molecule-1 in hepatocellular carcinoma.  

PubMed

Serum levels of circulating intercellular adhesion molecule-1 (cICAM-1) were measured in 23 patients with chronic hepatitis (CH), 22 with liver cirrhosis (LC) and 45 with hepatocellular carcinoma (HCC) using an ELISA. Serum samples from all patients showed significantly higher cICAM-1 levels than serum from 50 normal controls. The cICAM-1 level was significantly increased in LC or HCC when compared with CH, but no differences were noted between LC and HCC. Levels of cICAM-1 correlated well with serum bilirubin, retention rate of indocyanine green, hyaluronic acid, type IV collagen 7-S and type III procollagen peptide levels but not with tumor size or circulating tumor markers (alpha-fetoprotein and des-gamma-carboxyprothrombin). Our findings indicate that the measurement of cICAM-1 is useful for the determination of the severity of liver disease and hepatic fibrosis. HCC tissues obtained from 10 patients were immunohistochemically stained for ICAM-1. Enhanced ICAM-1 expression was found on the tumor cell membranes. Sequential measurements of cICAM-1 levels showed that they changed in a similar manner to those of alpha-fetoprotein during the course of treatment of HCC in a patient with very high pretreatment levels of both markers. These results suggest that HCC cells shed ICAM-1 into the circulation. We conclude that cICAM-1 is not a diagnostic marker for HCC, but may be useful for monitoring the response to treatment. PMID:7503959

Hyodo, I; Jinno, K; Tanimizu, M; Hosokawa, Y; Nishikawa, Y; Akiyama, M; Mandai, K; Moriwaki, S

1993-11-11

26

Reduced expression of intercellular adhesion molecule-1 in ovarian adenocarcinomas  

PubMed Central

Ovarian adenocarcinomas develop as the result of multiple genetic and epigenetic changes in the precursor ovarian surface epithelial (OSE) cells which result in a malignant phenotype. We investigated changes in gene expression in ovarian adenocarcinoma using a cDNA array containing 588 known human genes. We found that intercellular adhesion molecule-1 (ICAM-1) was expressed at lower levels in the ovarian tumour cell lines OAW42, PEO1 and JAM than in the immortalised human ovarian surface epithelial cell line HOSE 17.1. Further investigation revealed ICAM-1 was expressed in the surface epithelium of normal ovaries and both mRNA and protein expression levels were reduced in the majority of ovarian adenocarcinoma cell lines and primary tumours. ICAM-1 expression was increased in 8/8 cell lines treated with the de novo methyltransferase inhibitor 5-aza-2?-deoxycytidine, indicating that methylation of CpG islands may play a role in the down-regulation of its expression in primary tumours. There was a significant association between patients whose tumours expressed ICAM-1 and survival (P= 0.03), suggesting that expression levels of ICAM-1 may have clinical relevance. © 2001 Cancer Research Campaign

Arnold, J M; Cummings, M; Purdie, D; Chenevix-Trench, G

2001-01-01

27

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

28

Elevated levels of soluble adhesion molecules in sera of patients with acute bronchiolitis  

Microsoft Academic Search

The mechanisms of migration of neutrophils into the airway lumen are crucial in the development of airway injury of acute bronchiolitis and are mediated by adhesion molecules. In this study, we have attempted to evaluate the role of serum concentrations of the soluble form of intercellular adhesion molecule-1 (sICAM-1) in the disease activity in acute bronchiolitis and in respiratory syncytial

Chou-Cheng Lai; Hsiao-Yun Tai; Horng-Der Shen; Wen-Ting Chung; Ruey-Lung Chung; Ren-Bin Tang

29

Soluble intercellular adhesion molecule and C-reactive protein as early markers of infection in newborns.  

PubMed

In order to find a reliable early marker of infection in newborns a study with simultaneous determination of soluble Intercellular Adhesion Molecule-1 (sICAM-1) and C-Reactive Protein (CRP) was planned. Prospectively 90 babies < 5 days of age suspect of infection were included. Retrospectively this population was classified into an "infected" group (n = 45) and a "non-infected" group (n = 45). For each of these two groups we calculated the sensitivity, specificity and predictive values of sICAM-1 and CRP as early markers of infection. We determined the best cut-off level for sICAM-1 to be 300 micrograms/l and for CRP 5 mg/l. As a biochemical test for infection in the newborns the sensitivity and negative predictive value for CRP were 0.69 and 0.73 respectively. When sICAM-1 was added and CRP and s-ICAM-1 were used in combination the sensitivity improved significantly to 0.93, p < 0.01 and the negative predictive value improved to 0.92, p < 0.05. In normal 5-8 days old babies' sICAM-1 was significantly higher than at birth (cord blood), p < 0.0001. In conclusion, sICAM-1 and CRP in combination are better than CRP as a primary test for identification of infection in babies < 5 days of age. PMID:10875093

Hansen, A B; Verder, H; Staun-Olsen, P

2000-01-01

30

The Critical Role of Intercellular Adhesion Molecule1 in Masugi Nephritis in Rats  

Microsoft Academic Search

Intercellular adhesion molecule-1 (ICAM-1, CD54), an adhesion molecule of the immunoglobulin superfamily, is an endothelial cell surface ligand for such leukocyte integrins as lymphocyte-function-associated molecule 1 (LFA-1, CD 11 a\\/CD 18), Mac-1 (CDl lb\\/CD 18) and CD43. These molecules mediate adhesive interactions between leukocytes and endothelial cells and are critically involved in infiltration of leukocytes into inflammatory lesions. We examined

Jun Wada; Kenichi Shikata; Hirofumi Makino; Shigeru Morioka; Kyoji Hirata; Kosuke Ota; Takuya Tamatani; Masayuki Miyasaka; Tadashi Horiuchi; Sumihare Noji; Kiyoshi Nishikawa; Fumio Myokai; Shigehiko Taniguchi; Yashpal S. Kanwar; Zensuke Ota

1996-01-01

31

A prospective study of the sensitivity, specificity and diagnostic performance of soluble intercellular adhesion molecule 1, highly sensitive C-reactive protein, soluble E-selectin and serum amyloid A in the diagnosis of neonatal infection  

PubMed Central

Background Diagnosis of neonatal infection is difficult, because of it's non-specific clinical presentation and the lack of reliable diagnostic tests. The purpose of this study was to examine the potential diagnostic value of serum soluble intercellular adhesion molecule-1 (sICAM-1), soluble E-selectin (sE-selectin), highly sensitive C-reactive protein (hsCRP) and serum amyloid A (SAA) measurements, both individually and in combination in the setting of a neonatal intensive care unit. Methods 219 consecutive serum samples were taken from 149 infants undergoing sepsis work up in a neonatal intensive care unit. Clinical diagnosis was established in a prospective manner, blind to the results of the study measurements. Infants were classified by an experienced paediatrician as infected or not-infected, one week after presentation. Classification was based on clinical presentation, routine laboratory and radiological investigations and response to therapy. The infected group were sub-classified as (a) culture positive infection or (b) culture negative infection. sICAM-1, sE-selectin, hsCRP and SAA levels were determined from stored serum samples after diagnosis was established. Further sub-group analysis of results was undertaken according to early or late onset of infection and preterm or term status. Statistical analysis utilised Mann Whitney U test and ROC curve analysis. Results There were significantly increased serum levels of sICAM-1, hsCRP, E selectin (p < 0.001) and SAA (p = 0.004) in infected infants compared with non-infected. ROC curve analysis indicated area under the curve values of 0.79 (sICAM-1), 0.73 (hsCRP), 0.72 (sE-selectin) and 0.61 (SAA). ROC curve analysis also defined optimum diagnostic cut-off levels for each measurement. The performance characteristics of sICAM-1, hsCRP and sE-selectin included a high negative predictive value (NPV) for culture positive infection and this was enhanced by combination of all 4 measurements. Clinical subgroup analysis suggested particularly high NPV for early onset symptoms, however further studies are required to elucidate this finding. Conclusions All four study measurements demonstrated some diagnostic value for neonatal infection however sICAM-1, hsCRP and sE-selectin demonstrated the highest NPV individually. The optimum diagnostic cut off level for hsCRP measurement in this study was much lower than currently used in routine clinical practice. Use of a combination of measurements enhanced diagnostic performance, demonstrating sensitivity of 90.3% and NPV of 91.3%. This study suggests there may be value in use of several of these markers, individually and in combination to assist in excluding neonatal infection. Further work is needed to confirm a specific role in the exclusion of early onset infection.

2010-01-01

32

Circulating Adhesion Molecules in Humans Role of Hyperglycemia and Hyperinsulinemia  

Microsoft Academic Search

Background—We assessed the role of glucose and insulin in the regulation of circulating levels of soluble intercellular adhesion molecule-1 (sICAM-1) and vascular adhesion molecule-1 (sVCAM-1) in normal subjects and in patients with type 2 diabetes. Methods and Results—Plasma glucose concentrations were acutely raised in 10 normal subjects and 10 newly diagnosed, complication-free type 2 diabetic patients and maintained at 15

Raffaele Marfella; Katherine Esposito; Riccardo Giunta; Giuseppe Coppola; Lorenita De Angelis; Bartolomeo Farzati; Giuseppe Paolisso; Dario Giugliano

33

A truncated recombinant intercellular adhesion molecule-1 inhibits adhesion of leukemic cell lines to upregulated endothelial cells  

Microsoft Academic Search

Summary  Intercellular adhesion molecule-1, a member of the immunoglobulin supergene family, is the ligand for the integrin lymphocyte\\u000a function associated antigen-1. Intercellular adhesion molecule-1 and lymphocyte function associated antigen-1 binding interactions\\u000a mediate leukocyte adherence and migration. Previous work has shown that the adherence of lymphocyte function associated antigen-1\\u000a is directed to the first immunoglobulinlike domain of the endothelial cell surface protein

Lisa Ross; Cynthia M. Davis; Leslie Molony

1994-01-01

34

Light stimulates IFN?-Mediated intercellular adhesion molecule-1 upregulation of cancer cells  

Microsoft Academic Search

Intercellular adhesion molecule-1 (ICAM-1) works as one of the ligands for activating the killing activity of natural killer (NK) cells and cancer specific cytotoxic T lymphocytes (CTL). Expression of ICAM-1 enhances lymphocyte adhesion to the cancer cells in vivo. Cancer cell lines express significantly lower level of ICAM-1 than that of normal epithelium or benign cells. Overexpression of LIGHT (LIGHT:

Manchao Zhang; Ribo Guo; Yifan Zhai; Xin-Yuan Fu; Dajun Yang

2003-01-01

35

Conditional Vascular Cell Adhesion Molecule 1 Deletion in Mice  

PubMed Central

We generated vascular cell adhesion molecule (VCAM)-1 “knock-in” mice and Cre recombinase transgenic mice to delete the VCAM-1 gene (vcam-1) in whole mice, thereby overcoming the embryonic lethality seen with conventional vcam-1–deficient mice. vcam-1 knock-in mice expressed normal levels of VCAM-1 but showed loss of VCAM-1 on endothelial and hematopoietic cells when interbred with a “TIE2Cre” transgene. Analysis of peripheral blood from conditional vcam-1–deficient mice revealed mild leukocytosis, including elevated immature B cell numbers. Conversely, the bone marrow (BM) had reduced immature B cell numbers, but normal numbers of pro-B cells. vcam-1–deficient mice also had reduced mature IgD+ B and T cells in BM and a greatly reduced capacity to support short-term migration of transferred B cells, CD4+ T cells, CD8+ T cells, and preactivated CD4+ T cells to the BM. Thus, we report an until now unappreciated dominant role for VCAM-1 in lymphocyte homing to BM.

Koni, Pandelakis A.; Joshi, Sunil K.; Temann, Ulla-Angela; Olson, Dian; Burkly, Linda; Flavell, Richard A.

2001-01-01

36

Migration inhibitory factor up-regulates vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 via Src, PI3 kinase, and NF?B  

PubMed Central

Cell adhesion molecules are critical in monocyte (MN) recruitment in immune-mediated and hematologic diseases. We investigated the novel role of recombinant human migration inhibitory factor (rhMIF) in up-regulating vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) and their signaling pathways in human MNs. rhMIF-induced expression of VCAM-1 and ICAM-1 was significantly higher compared with nonstimulated MNs. rhMIF induced MN VCAM-1 and ICAM-1 expression in a concentration-dependent manner (P < .05). Antisense oligodeoxynucleotides (ODNs) and inhibitors of Src, PI3K, p38, and NF?B significantly reduced rhMIF-induced MN VCAM-1 and ICAM-1 expression (P < .05). However, Erk1/2 and Jak2 were not involved. Silencing RNA directed against MIF, and inhibitors of Src, PI3K, NF?B, anti–VCAM-1, and anti–ICAM-1 significantly inhibited rhMIF-induced adhesion of HL-60 cells to human dermal microvascular endothelial cells (HMVECs) or an endothelial cell line, HMEC-1, in cell adhesion assays, suggesting the functional significance of MIF-induced adhesion molecules (P < .05). rhMIF also activated MN phospho-Src, -Akt, and -NF?B in a time-dependent manner. rhMIF induced VCAM-1 and ICAM-1 up-regulation in 12 hours via Src, PI3K, and NF?B as shown by Western blotting and immunofluorescence. MIF and MIF-dependent signaling pathways may be a potential target for treating diseases characterized by up-regulation of cell adhesion molecules.

Amin, M. Asif; Haas, Christian S.; Zhu, Kui; Mansfield, Pamela J.; Kim, Michael J.; Lackowski, Nicholas P.; Koch, Alisa E.

2006-01-01

37

Significance of platelet endothelial cell adhesion molecule-1 (PECAM-1) and intercellular adhesion molecule-1 (ICAM-1) expressions in preeclamptic placentae.  

PubMed

Although preeclampsia (PE) is one of the most important problems affecting pregnant women, etiologic factors in its development are still unclear. We aimed to investigate the expression levels of platelet endothelial cell adhesion molecule-1 (PECAM-1) and intercellular adhesion molecule-1 (ICAM-1) in preeclamptic and control healthy placentas. Placental tissue samples were obtained after delivery from patients diagnosed with PE, and from normal term pregnants and analyzed by immunohistochemistry for the expression levels of the two adhesion molecules PECAM-1 and ICAM-1. A strong expression of PECAM-1 in endothelial cells lining the vessel walls of placental villi in placentas of control group was found, but the intensity of PECAM-1 expression was highly reduced in placentas of PE group (p = 0.017). Conversely, a strong expression of ICAM-1 was observed in placental villi in PE, significantly higher than that of normal placentas (p = 0.005). The findings of a decrease of PECAM-1 expression and an increase of ICAM-1 expression in preeclamptic placenta suggest the existence of functional roles of these adhesion molecules in the pathophysiology of PE, probably by contributing to the reduced trophoblast invasion and the increased vascular damage, respectively. Inhibiting ICAM-1 (i.e., with ICAM-1 monoclonal antibody) and promoting PECAM-1 expression may be good therapeutic approaches to prevent PE symptoms in the future. PMID:22396143

Goksu Erol, Azize Yasemin; Nazli, Mumtaz; Elis Yildiz, Sevda

2012-03-07

38

Curcumin attenuates TNF-?-induced expression of intercellular adhesion molecule-1, vascular cell adhesion molecule-1 and proinflammatory cytokines in human endometriotic stromal cells.  

PubMed

Curcumin, a naturally occurring polyphenolic compound from Curcuma longa, has long been used in folk medicine as an antiinflammatory remedy in Asian countries. Endometriosis is a chronic gynecological inflammatory disorder in which immune system deregulation may play a role in its initiation and progression. A number of mediators, including cell adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1); proinflammatory cytokines such as tumour necrosis factor-? (TNF-?), interleukin-1 (IL-1), IL-6 and IL-8; and chemokines such as monocyte chemotactic protein-1 (MCP-1), play key roles in the pathogenesis of endometriosis. The aim of our study was to explore the effect of curcumin on the expression of these critical molecules in human ectopic endometriotic stromal cells isolated from women with endometriosis. Endometriotic stromal cells treated with curcumin showed marked suppression of TNF-?-induced mRNA expression of ICAM-1 and VCAM-1. Curcumin treatment also significantly decreased the TNF-?-induced cell surface and total protein expression of ICAM-1 and VCAM-1 in a dose-dependent manner. In addition, treatment of endometriotic stromal cells with curcumin markedly inhibited TNF-?-induced secretion of IL-6, IL-8 and MCP-1. Furthermore, curcumin inhibited the activation of transcription factor NF-?B, a key regulator of inflammation, in human endometriotic stromal cells. These findings suggest that curcumin may have potential therapeutic uses in the prevention and treatment of endometriosis. PMID:22183741

Kim, Ki-Hyung; Lee, Eun Na; Park, Jin Kyeong; Lee, Ja-Rang; Kim, Ji-Hyun; Choi, Hak-Jong; Kim, Bong-Seon; Lee, Hee-Woo; Lee, Kyu-Sup; Yoon, Sik

2011-12-20

39

Prevalence of the K469E polymorphism of intercellular adhesion molecule 1 gene in Italian patients with inflammatory bowel disease  

Microsoft Academic Search

Background. Intercellular adhesion molecule 1 plays an important role in the recruitment of leucocytes at sites of inflammation and is up-regulated in intestinal mucosa of inflammatory bowel disease. Intercellular adhesion molecule 1 gene lies on chromosome 19p13, implicated in determining susceptibility to inflammatory bowel disease. Recently, the polymorphism K469E of intercellular adhesion molecule 1 gene has been identified.Aim. To assess

A Papa; R Pola; A Flex; S Danese; A Armuzzi; E Gaetani; L Guidi; I De Vitis; R Urgesi; A Grillo; M Serricchio; A. S Proia; G Fedeli; G Gasbarrini; P Pola; A Gasbarrini

2004-01-01

40

Intercellular adhesion molecule-1 (ICAM-1; CD54) expression in human hepatocytic cells depends on protein kinase C  

Microsoft Academic Search

Background\\/Aims: Intracellular regulation of intercellular adhesion molecule-1 has mainly been studied in lymphoid, endothelial, and epithelial cells. Intercellular adhesion molecule-1 plays a central role in many immune responses, and we have previously studied its regulation in hepatocytes. Here we report how manipulation of intracellular signal systems influenced its expression.Methods: The constitutive and cytokine-induced expression of intercellular adhesion molecule-1 mRNA and

Dag Kvale; Randi Holme

1996-01-01

41

Increased binding of synovial T lymphocytes from rheumatoid arthritis to endothelial-leukocyte adhesion molecule-1 (ELAM-1) and vascular cell adhesion molecule-1 (VCAM-1).  

PubMed Central

The infiltration of the synovial membrane (SM) by mononuclear cells, mostly T cells, is a typical histopathological feature associated with rheumatoid arthritis (RA). The entry of T lymphocytes into the SM is believed to be mediated by a number of molecules in the endothelium that are induced in response to a series of inflammatory mediators. In this study, we have investigated the adhesion of synovial T cells from RA patients to two endothelial ligands: endothelial-leukocyte adhesion molecule-1 (ELAM-1), the only selectin known to function as a vascular addressin for T cells, and vascular cell adhesion molecule-1 (VCAM-1), the cellular ligand of VLA-4. Our results clearly demonstrate that synovial T cells isolated from both SM and synovial fluid (SF), bearing an activated and memory phenotype, displayed an enhanced capacity to interact with these two endothelial molecules as compared with T cells from peripheral blood (PB) either of the same RA patients or healthy donors. A further enhancement of VLA-4-mediated T cell binding to VCAM-1 and fibronectin could be observed when already in vivo-activated synovial T cells were stimulated in vitro with phorbol esters, suggesting the existence of several cellular affinity levels for both very late activation-4 (VLA-4) ligands. Moreover, both PB and synovial T cells from RA patients exhibited strong proliferative responses when they were cultured with either fibronectin or VCAM-1 in combination with submitogenic doses of anti-CD3 mAb. This increased endothelial binding ability of synovial T lymphocytes together with their proliferation in response to the interaction with VCAM-1 and fibronectin may represent important mechanisms in the regulation of T cell penetration and persistence in the chronically inflamed SM of RA. Images

Postigo, A A; Garcia-Vicuna, R; Diaz-Gonzalez, F; Arroyo, A G; De Landazuri, M O; Chi-Rosso, G; Lobb, R R; Laffon, A; Sanchez-Madrid, F

1992-01-01

42

Targeting sites of inflammation: intercellular adhesion molecule-1 as a target for novel inflammatory therapies  

PubMed Central

Targeted drug delivery to sites of inflammation will provide effective, precise, and safe therapeutic interventions for treatment of diverse disease conditions, by limiting toxic side effects and/or increasing drug action. Disease-site targeting is believed to play a major role in the enhanced efficacy observed for a variety of drugs when formulated inside lipid vesicles. This article will focus on the factors and mechanisms involved in drug targeting to sites of inflammation and the importance of cell adhesion molecules, in particular intercellular adhesion molecule-1, in this process.

Hua, Susan

2013-01-01

43

Increase in the adhesion molecule P-selectin in endothelium overlying atherosclerotic plaques. Coexpression with intercellular adhesion molecule-1.  

PubMed Central

P-selectin (GMP-140) is an adhesion molecule present within endothelial cells that is rapidly translocated to the cell membrane upon activation, where it mediates endothelial-leukocyte interactions. Immunohistochemical analysis of human atherosclerotic plaques has shown strong expression of P-selectin by the endothelium overlying active atherosclerotic plaques. P-selectin is not, however, detected in normal arterial endothelium or in endothelium overlying inactive fibrous plaques. Color image analysis was used to quantitate the degree of P-selectin expression in the endothelium and demonstrates a statistically significant increase in P-selectin expression by atherosclerotic endothelial cells. Double immunofluorescence shows that some of this P-selectin is expressed on the luminal surface of the endothelial cells. Previous work has demonstrated a significant up-regulation in the expression of the intercellular adhesion molecule-1 in atherosclerotic endothelium and a study on the expression of intercellular adhesion molecule-1 and P-selectin in atherosclerosis shows a highly positive correlation. These results suggest that the selective and cooperative expression of P-selectin and intercellular adhesion molecule-1 may be involved in the recruitment of monocytes into sites of atherosclerosis. Images Figure 1 Figure 3 Figure 4 Figure 5

Johnson-Tidey, R. R.; McGregor, J. L.; Taylor, P. R.; Poston, R. N.

1994-01-01

44

Involvement of Platelet-Endothelial Cell Adhesion Molecule1 in Neutrophil Recruitment in Vivo  

Microsoft Academic Search

During inflammation, neutrophils migrate from the vascular lumen into extravascular sites. In vitro assays have suggested that platelet-endothelial cell adhesion molecule-1 [PECAM-1 (CD31)], a member of the immunoglobulin superfamily, is required for the transmigration of neutrophils across endothelial monolayers. Antibody to human PECAM-1, which cross-reacts with rat PECAM-1, was found to block not only in vivo accumulation of rat neutrophils

Ara A. Vaporciyan; Horace M. Delisser; Horng-Chin Yan; Ignacio I. Mendiguren; Stephen R. Thom; Michael L. Jones; Peter A. Ward; Steven M. Albelda

1993-01-01

45

Intercellular adhesion molecule-1 K469E gene polymorphism and Alzheimer’s disease  

Microsoft Academic Search

Inflammatory processes are considered important in the pathogenesis of Alzheimer’s disease (AD). Intercellular adhesion molecule-1 (ICAM-1) is an important mediator of inflammatory response and immune cell activation, is expressed on cerebrovascular endothelium and neuritic plaques in brain of AD patients, and seems to be implicated in the process of neuro-degeneration. A common polymorphism of the ICAM-1 gene (K469E) has been

Roberto Pola; Andrea Flex; Eleonora Gaetani; Angelo Santoliquido; Michele Serricchio; Paolo Pola; Roberto Bernabei

2003-01-01

46

Carcinoembryonic Antigen-Related Cell Adhesion Molecule 1 Inhibits Proximal TCR Signaling by Targeting ZAP701  

Microsoft Academic Search

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

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

47

Intercellular Adhesion Molecule1 and Interleukin6 Gene Polymorphisms in Patients with Advanced-Stage Endometriosis  

Microsoft Academic Search

Background\\/Aims: The aim of this study was to investigate the possibility that the K469E and G241R polymorphisms in the intercellular adhesion molecule-1 (ICAM-1) gene and the C-634G polymorphism in the interleukin (IL)-6 gene are associated with endometriosis in the Korean population. Methods: The ICAM-1 gene K469E and G241R polymorphisms and the IL-6 gene C-634G polymorphism were evaluated in 390 patients

Soo Jin Chae; Gyoung Hoon Lee; Young Min Choi; Min A Hong; Jong Mee Kim; Kyu Sup Lee; Seung Yup Ku; Shin Yong Moon

2010-01-01

48

Transcriptional Regulation of Intercellular Adhesion Molecule1: PMA-Induction Is Mediated by NF?B  

Microsoft Academic Search

The surface glycoprotein intercellular adhesion molecule-1 (ICAM-1) mediates important immunologic cell interactions during cutaneous inflammatory processes by binding to the leukocyte integrin lymphocyte function-associated antigen-1. The expression of ICAM-1 is induced in epidermal keratinoeytes by certain pro-inflammatory stimuli, and this modulation is transcriptionally regulated. To identify the molecular mechanisms involved in the regulation of 1CAMA gene expression, we have previously

Stefan Müller; Claudia Kamrnerbauer; Uta Simous; Naotaka Shibagaki; Lian-Jie Li; S. Wright Caughman; Klaus Degitz

1995-01-01

49

Potential value of urinary intercellular adhesion molecule-1 determination in patients with bladder cancer  

Microsoft Academic Search

Objectives. Intercellular adhesion molecule-1 (ICAM-1) is known to play a role in immunity against bladder cancer and can be detected in the supernatants of cultured bladder cancer cells that constitutively express ICAM-1. This study was performed to examine the relevance of the ICAM-1 urine test in patients with bladder cancer.Methods. A total of 53 patients with bladder carcinoma, 35 with

Nan-Haw Chow; Chih-Jen Cheng; Yun-Chan Chi; Hsiao-Shen Liu; Tzong-Shin Tzai; Johnny Shinn-Nan Lin

1998-01-01

50

Molecular regulation of intercellular adhesion molecule 1 (ICAM-1) expression in renal cell carcinoma  

Microsoft Academic Search

Intercellular adhesion molecule-1 (ICAM-1) mediates two important functional. aspects of tumor biology, namely enhancement of tumor metastasis and mediation of host defense mechanisms such as lymphocyte-mediated tumor cytotoxicity. Since ICAM-1 is expressed by most renal cell carcinomas (RCC), the regulation of ICAM-1 expression is important in understanding the biological behavior of RCC. We report an investigation on ICAM-1 expression and

K. Tanabe; S. C. Campbell; J. P. Alexander; F. Steinbach; M. G. Edinger; R. R. Tubbs; A. C. Novick; E. A. Klein

1997-01-01

51

The intercellular adhesion molecule-1 K469E polymorphism in type 1 diabetes  

Microsoft Academic Search

Type 1 (insulin-dependent) diabetes is a complex trait. The region harboring the ICAM1 gene on 19p13 links to type 1 diabetes, and a growing body of evidence indicates that intercellular adhesion molecule-1 (ICAM-1) could play a role in type 1 diabetes development. Recently, association studies of an ICAM-1 K469E polymorphism in type 1 diabetes populations have reported conflicting results. Hence,

Ole. P. Kristiansen; Runa L. Nolsøe; Heidi Holst; Sine Reker; Zenia M. Larsen; Jesper Johannesen; Jørn Nerup; Flemming Pociot; Thomas Mandrup-Poulsen

2000-01-01

52

Indomethacin induced gastropathy in CD18, intercellular adhesion molecule 1, or P-selectin deficient mice  

PubMed Central

BACKGROUND—Neutrophil-endothelial cell interactions are thought to play a critical role in the pathophysiology of non-steroidal anti-inflammatory drug (NSAID) induced gastropathy.?AIMS—To optimise a mouse model of NSAID induced gastropathy and to evaluate the importance of adhesion molecules using adhesion molecule deficient mice.?METHODS—Gastropathy was induced in C57BL/6 mice or their adhesion molecule deficient counterparts via oral administration of indomethacin (20 mg/kg). Lesion scores, mucosal permeability, and histopathology were used to assess gastric mucosal injury.?RESULTS—Intragastric administration of indomethacin induced linear haemorrhagic mucosal lesions, primarily in the corpus of the stomach that were first observed at six hours. These lesions continued to develop over the next six hours with maximal lesion scores and mucosal permeabilities at 12 hours. When indomethacin was administered to mice deficient in CD18, intercellular adhesion molecule 1 (ICAM-1), or P-selectin, there were significant decreases in lesion scores compared with their C57BL/6 controls. In addition, mucosal permeabilities were found to be significantly lower in CD18 or ICAM-1 deficient mice observed at 12 hours.?CONCLUSION—Certain leucocyte and endothelial cell adhesion molecules are important determinants for full expression of indomethacin induced gastropathy. It is proposed that this modification of the mouse model may be useful for the investigation of other pathophysiological mechanisms of NSAID induced gastropathy.???Keywords: indomethacin; gastropathy; cyclooxygenase; intercellular adhesion molecule; VCAM; vascular cell adhesion molecule; P-selectin

Morise, Z; Granger, D; Fuseler, J; Anderson, D; Grisham, M

1999-01-01

53

Expression of Adhesion Molecules and G Proteins in Circulating Neutrophils in Chronic Obstructive Pulmonary Disease  

Microsoft Academic Search

We investigated the expression of adhesion molecules in circulating neutrophils (lymphocyte func- tion-associated antigen-1 (LFA-1), Mac-1, and L-selectin) and endothelial cells (soluble intercellular adhesion molecule-1(sICAM-1)) in 23 patients with stable chronic obstructive pulmonary disease (COPD), 18 subjects with exacerbated COPD, and 23 healthy volunteers. Also, in these circulating neutrophils, we assessed the expression of two G protein subunits (G a

AINA NOGUERA; XAVIER BUSQUETS; JAUME SAULEDA; JOSE M. VILLAVERDE; ALVAR G. N. AGUSTÍ; Carmen Santos

1998-01-01

54

A dimeric crystal structure for the N-terminal two domains of intercellular adhesion molecule-1  

PubMed Central

The 3.0-? structure of a 190-residue fragment of intercellular adhesion molecule-1 (ICAM-1, CD54) reveals two tandem Ig-superfamily (IgSF) domains. Each of two independent molecules dimerizes identically with a symmetry-related molecule over a hydrophobic interface on the BED sheet of domain 1, in agreement with dimerization of ICAM-1 on the cell surface. The residues that bind to the integrin LFA-1 are well oriented for bivalent binding in the dimer, with the critical Glu-34 residues pointing away from each other on the periphery. Residues that bind to rhinovirus are in the flexible BC and FG loops at the tip of domain 1, and these and the upper half of domain 1 are well exposed in the dimer for docking to virus. By contrast, a residue important for binding to Plasmodium falciparum-infected erythrocytes is in the dimer interface. The presence of A? strands in both domains 1 and 2, conserved hydrogen bonds at domain junctions, and elaborate hydrogen bond networks around the key integrin binding residues in domain 1 make these domains suited to resist tensile forces during adhesive interactions. A subdivision of the intermediate (I) set of IgSF domains is proposed in which domain 1 of ICAM-1 and previously described I set domains belong to the I1 set and domain 2 of ICAM-1, ICAM-2, and vascular cell adhesion molecule-1 belong to the I2 set.

Casasnovas, Jose M.; Stehle, Thilo; Liu, Jin-huan; Wang, Jia-huai; Springer, Timothy A.

1998-01-01

55

Endothelial cell injury in cardiac surgery: salicylate may be protective by reducing expression of endothelial adhesion molecules1  

Microsoft Academic Search

Objective: Cardiac surgery with cardiopulmonary bypass induces ischemia to the heart, hypoxemia to various tissues and release of endotoxins. The endothelial cell may suffer from hypoxia and trigger cascades of adverse reactions by activation of neutrophils through adhesion molecules. The authors measured expression of intercellular adhesion molecule-1 (ICAM-1), during hypoxia and normoxia and hypothesized that salicylate, which inhibits the nuclear

Gregor Zun; Andrea L. Dzus; Urs Niederhauser; Paul Vogt; Marko Turina

56

CCN4 induces vascular cell adhesion molecule-1 expression in human synovial fibroblasts and promotes monocyte adhesion.  

PubMed

CCN4 is a cysteine-rich protein that belongs to the Cyr61, CTGF, Nov family of matricellular proteins. Here, we investigated the intracellular signaling pathways involved in CCN4-induced vascular cell adhesion molecule-1 expression in human osteoarthritis synovial fibroblasts. Stimulation of OASFs with CCN4 induced VCAM-1 expression. CCN4-induced VCAM-1 expression was attenuated by ?v?5 or ?6?1 integrin antibody, Syk inhibitor, PKC? inhibitor (rottlerin), JNK inhibitor (SP600125), and AP-1 inhibitors (curcumin and tanshinone). Stimulation of cells with CCN4 increased Syk, PKC?, and JNK activation. Treatment of OASFs with CCN4 also increased c-Jun phosphorylation, AP-1-luciferase activity, and c-Jun binding to the AP-1 element in the VCAM-1 promoter. Moreover, up-regulation of VCAM-1 increased the adhesion of monocytes to OASF monolayers, and this adhesion was attenuated by transfection with a VCAM-1 siRNA. Our results suggest that CCN4 increases VCAM-1 expression in human OASFs via the Syk, PKC?, JNK, c-Jun, and AP-1 signaling pathways. The CCN4-induced VCAM-1 expression promoted monocyte adhesion to human OASFs. PMID:23313051

Liu, Ju-Fang; Hou, Sheng-Mou; Tsai, Chun-Hao; Huang, Chun-Yin; Hsu, Chin-Jung; Tang, Chih-Hsin

2013-01-08

57

Regulation by Fibrinogen and Its Products of Intercellular Adhesion Molecule1 Expression in Human Saphenous Vein Endothelial Cells  

Microsoft Academic Search

It has been reported that fibrinogen may act as a bridging ligand, binding to intercellular adhesion molecule-1 (ICAM-1) on human umbilical vein endothelial cells and to Mac-1 on THP-1 cells (a monocytic cell line) to increase adhesion. In this study, we investigated whether fibrinogen altered the expression of ICAM-1 and, thus, increased the adhesion of THP-1 cells to cultured human

Suzanne L. Harley; Justin Sturge; Janet T. Powell

2010-01-01

58

Synovial fluid levels of E-selectin and intercellular adhesion molecule-1: relationship to joint inflammation in children with chronic arthritis.  

PubMed

E-selectin and intercellular adhesion molecule (ICAM)-1 are crucial to the inflammatory response in chronic inflammatory arthritis. Soluble (s) levels of these molecules in sera and synovial fluid (SF) correlate with some clinical parameters and synovial tissue expression of the same molecules in rheumatoid arthritis. Studies of sera from children with chronic inflammatory arthritis corroborate this information; corresponding SF data are relatively lacking. We thus studied SF sE-selectin and sICAM-1 in 28 children with active juvenile rheumatoid arthritis or a spondyloarthropathy. Levels were correlated with erythrocyte sedimentation rate (ESR), SF leukocyte counts, duration of disease, and duration of response to concomitant intra-articular corticosteroid injection. Levels were compared according to use of methotrexate and/or sulfasalazine. Synovial fluid sE-selectin correlated with ESR and SF leukocyte counts. There was a trend toward lower sICAM-1 in patients treated with sulfasalazine and/or methotrexate. We conclude that SF levels of sE-selectin accurately reflect intra-synovial inflammation. Soluble ICAM-1 levels may reflect the effects of disease-modifying agents. PMID:12215860

Bloom, Bradley J; Nelson, Sarah M; Alario, Anthony J; Miller, Laurie C; Schaller, Jane G

2002-06-07

59

[Expression of vascular cell adhesion molecule-1 in patients with multiple myeloma and its significance].  

PubMed

In order to investigate the expression of vascular cell adhesion molecule-1 (VCAM-1) in patients with multiple myeloma and its significance, the expression of VCAM-1 in 23 patients were detected by reverse transcription-PCR (RT-PCR) and then compared with that in normal control. The results showed that the expression of VCAM-1 in patients with newly diagnosed and relapsed/refractory multiple myeloma was much higher than that in normal control and in patients reached plateau stage (p < 0.05). There was no statistically significant difference between newly diagnosed and relapsed/refractory patients (p > 0.05). It is concluded that the expression of VCAM-1 in patients with multiple myeloma is abnormal, which may be an important factor for the pathogenesis of multiple myeloma. PMID:19379571

Liu, Zeng-Yan; Lu, Hua; Liu, Peng; Chen, Li-Juan; Wang, Li-Xia; Lu, Shi-Feng; Li, Jian-Yong

2009-04-01

60

Circulating soluble adhesion molecules E-cadherin, E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in patients with gastric cancer.  

PubMed Central

The concentrations of the soluble adhesion molecules E-cadherin, E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) were investigated in 45 patients with gastric cancer before treatment and their correlation with clinical, histological and routine laboratory parameters was examined. Data were collected on tumour stage at presentation, presence and sites of metastatic disease, tumour pathology, survival and results of routine laboratory tests. Serum concentrations of ICAM-1 and VCAM-1 were significantly elevated in the patients with gastric cancer in comparison with the group of healthy subjects (P < 0.00001 and P < 0.0001 respectively). Increased serum concentrations of VCAM-1 were associated with locally advanced and metastatic disease whereas ICAM-1 was significantly elevated both in local and in advanced/metastatic disease. Soluble E-cadherin and E-selectin concentrations did not show any significant elevation in gastric cancer patients. Concentrations of soluble adhesion molecules showed significant correlation with each other (except E-selectin and VCAM-1) and with alkaline phosphatase. Soluble ICAM-1 and VCAM-1 were significantly associated with an elevated total white cell count. Patients with elevated VCAM-1 had significantly poorer survival in comparison with patients with normal serum levels (P = 0.0361). Images Figure 1 Figure 2

Velikova, G.; Banks, R. E.; Gearing, A.; Hemingway, I.; Forbes, M. A.; Preston, S. R.; Jones, M.; Wyatt, J.; Miller, K.; Ward, U.; Al-Maskatti, J.; Singh, S. M.; Ambrose, N. S.; Primrose, J. N.; Selby, P. J.

1997-01-01

61

Platelet Endothelial Cell Adhesion Molecule1 and Vascular Endothelial Cadherin Cooperatively Regulate Fibroblast Growth Factor-induced Modulations of Adherens Junction Functions  

Microsoft Academic Search

Cellular adherens junctions are formed by cadherins linked to proteins of the catenin family. In endothelial cells, not only vascular endothelial cadherin but also platelet endothelial cell adhesion molecule-1 localizes into junctions and associates with ?-catenin. To explore a putative cooperation of platelet endothelial cell adhesion molecule-1 and vascular endothelial cadherin, we analyzed transfectants expressing either platelet endothelial cell adhesion

Thomas Halama; Marion Gröger; Manuela Pillinger; Günther Staffler; Elisabeth Prager; Hannes Stockinger; Wolfgang Holnthoner; Sonja Lechleitner; Klaus Wolff; Peter Petzelbauer

2001-01-01

62

Endothelial targeting of high-affinity multivalent polymer nanocarriers directed to intercellular adhesion molecule 1.  

PubMed

Targeting of diagnostic and therapeutic agents to endothelial cells (ECs) provides an avenue to improve treatment of many maladies. For example, intercellular adhesion molecule 1 (ICAM-1), a constitutive endothelial cell adhesion molecule up-regulated in many diseases, is a good determinant for endothelial targeting of therapeutic enzymes and polymer nanocarriers (PNCs) conjugated with anti-ICAM (anti-ICAM/PNCs). However, intrinsic and extrinsic factors that control targeting of anti-ICAM/PNCs to ECs (e.g., anti-ICAM affinity and PNC valency and flow) have not been defined. In this study we tested in vitro and in vivo parameters of targeting to ECs of anti-ICAM/PNCs consisting of either prototype polystyrene or biodegradable poly(lactic-coglycolic) acid polymers (approximately 200 nm diameter spheres carrying approximately 200 anti-ICAM molecules). Anti-ICAM/PNCs, but not control IgG/PNCs 1) rapidly (t1/2 approximately 5 min) and specifically bound to tumor necrosis factor-activated ECs in a dose-dependent manner (Bmax approximately 350 PNC/cell) at both static and physiological shear stress conditions and 2) bound to ECs and accumulated in the pulmonary vasculature after i.v. injection in mice. Anti-ICAM/PNCs displayed markedly higher EC affinity versus naked anti-ICAM (Kd approximately 80 pM versus approximately 8 nM) in cell culture and, probably because of this factor, higher value (185.3 +/- 24.2 versus 50.5 +/- 1.5% injected dose/g) and selectivity (lung/blood ratio 81.0 +/- 10.9 versus 2.1 +/- 0.02, in part due to faster blood clearance) of pulmonary targeting. These results 1) show that reformatting monomolecular anti-ICAM into high-affinity multivalent PNCs boosts their vascular immuno-targeting, which withstands physiological hydrodynamics and 2) support potential anti-ICAM/PNCs utility for medical applications. PMID:16505161

Muro, Silvia; Dziubla, Thomas; Qiu, Weining; Leferovich, John; Cui, Xiumin; Berk, Erik; Muzykantov, Vladimir R

2006-02-27

63

Regulation of Bacteria-Induced Intercellular Adhesion Molecule-1 by CCAAT/Enhancer Binding Proteins  

PubMed Central

Direct interaction between bacteria and epithelial cells may initiate or amplify the airway response through induction of epithelial defense gene expression by nuclear factor-?B (NF-?B). However, multiple signaling pathways modify NF-?B effects to modulate gene expression. In this study, the effects of CCAAT/enhancer binding protein (C/EBP) family members on induction of the leukocyte adhesion glycoprotein intercellular adhesion molecule-1 (ICAM-1) was examined in primary cultures of human tracheobronchial epithelial cells incubated with nontypeable Haemophilus influenzae. Increased ICAM-1 gene transcription in response to H. influenzae required gene sequences located at ?200 to ?135 in the 5?-flanking region that contain a C/EBP-binding sequence immediately upstream of the NF-?B enhancer site. Constitutive C/EBP? was found to have an important role in epithelial cell ICAM-1 regulation, while the adjacent NF-?B sequence binds the RelA/p65 and NF-?B1/p50 members of the NF-?B family to induce ICAM-1 expression in response to H. influenzae. The expression of C/EBP proteins is not regulated by p38 mitogen-activated protein kinase activation, but p38 affects gene transcription by increasing the binding of TATA-binding protein to TATA-box–containing gene sequences. Epithelial cell ICAM-1 expression in response to H. influenzae was decreased by expressing dominant-negative protein or RNA interference against C/EBP?, confirming its role in ICAM-1 regulation. Although airway epithelial cells express multiple constitutive and inducible C/EBP family members that bind C/EBP sequences, the results indicate that C/EBP? plays a central role in modulation of NF-?B–dependent defense gene expression in human airway epithelial cells after exposure to H. influenzae.

Manzel, Lori J.; Chin, Cecilia L.; Behlke, Mark A.; Look, Dwight C.

2009-01-01

64

Detection of vascular adhesion molecule-1 expression using a novel multimodal nanoparticle.  

PubMed

Endothelial vascular adhesion molecule-1 (VCAM-1) is a critical component of the leukocyte-endothelial adhesion cascade, and its strict temporal and spatial regulation make it an ideal target for imaging and therapy. The goal of this study was to develop novel VCAM-1-targeted imaging agents detectable by MRI and fluorescence imaging using phage display-derived peptide sequences and multimodal nanoparticles (NPs). We hypothesized that VCAM-1-mediated cell internalization of phage display-selected peptides could be harnessed as an amplification strategy to chaperone and trap imaging agents inside VCAM-1-expressing cells, thus improving target-to-background ratios. To accomplish our goal, iterative phage display was performed on murine endothelium under physiological flow conditions to identify a family of VCAM-1-mediated cell-internalizing peptides. One specific sequence, containing the VHSPNKK motif that has homology to the alpha-chain of very late antigen (a known ligand for VCAM-1), was shown to bind VCAM-1 and block leukocyte-endothelial interactions. Compared with VCAM-1 monoclonal antibody, the peptide showed 12-fold higher target-to-background ratios. A VHSPNKK-modified magnetofluorescent NP (VNP) showed high affinity for endothelial cells expressing VCAM-1 but surprisingly low affinity for macrophages. In contrast, a control NP without VCAM-1-targeting sequences showed no affinity for endothelial cells. In vivo, VNP successfully identified VCAM-1-expressing endothelial cells in a murine tumor necrosis factor-alpha-induced inflammatory model and colocalized with VCAM-1-expressing cells in atherosclerotic lesions present in cholesterol-fed apolipoprotein E apoE-/- mice. These results indicate that: (1) small peptide sequences can significantly alter targeting of NPs, (2) the used amplification strategy of internalization results in high target-to-background ratios, and (3) this technology is useful for in vivo imaging of endothelial markers. PMID:15653572

Kelly, Kimberly A; Allport, Jennifer R; Tsourkas, Andrew; Shinde-Patil, Vivek R; Josephson, Lee; Weissleder, Ralph

2005-01-13

65

Light stimulates IFNgamma-mediated intercellular adhesion molecule-1 upregulation of cancer cells.  

PubMed

Intercellular adhesion molecule-1 (ICAM-1) works as one of the ligands for activating the killing activity of natural killer (NK) cells and cancer specific cytotoxic T lymphocytes (CTL). Expression of ICAM-1 enhances lymphocyte adhesion to the cancer cells in vivo. Cancer cell lines express significantly lower level of ICAM-1 than that of normal epithelium or benign cells. Overexpression of LIGHT (LIGHT: homologous to lymphotoxins, indicating inducible expression, and competes with herpes simplex virus glycoprotein D for herpes virus entry mediator [HVEM/TR2]) in MDA-MB-231 human breast cancer cells was observed to suppress tumor growth in vivo. In order to elucidate the mechanisms how LIGHT overexpression could trigger tumor suppression, the expression level of a panel of cell surface makers CD54, CD56, CD95, and CD119 was investigated in a group of cancer cells. Flow cytometry analysis results demonstrate that LIGHT gene expression in cancer cells can greatly increase ICAM-1 expression level, IFNgamma alone can stimulate cancer cells to express ICAM-1, which can be highly augmented by LIGHT in a dose-dependent manner. This upregulation of ICAM-1 expression is not only at ICAM-1 protein trafficking level on cell surface as demonstrated by flow cytometry analysis, but also at ICAM-1 total protein level as confirmed by Western blot. There is no difference of expression level among these cancer cell lines for the other three cell surface markers: CD56, CD95 (Fas), and CD119. It was confirmed that LIGHT enhancement upregulation of ICAM-1 expression is at least STAT1 and JAK1 dependent by using STAT1-deficient U3A and JAK1-deficient E2A4 cells. These findings suggest that LIGHT-induced inhibition of tumor growth is highly correlated with its upregulation of ICAM-1 expression. PMID:12651068

Zhang, Manchao; Guo, Ribo; Zhai, Yifan; Fu, Xin-Yuan; Yang, Dajun

2003-04-01

66

Intercellular adhesion molecule-1 K469E gene polymorphism and Alzheimer's disease.  

PubMed

Inflammatory processes are considered important in the pathogenesis of Alzheimer's disease (AD). Intercellular adhesion molecule-1 (ICAM-1) is an important mediator of inflammatory response and immune cell activation, is expressed on cerebrovascular endothelium and neuritic plaques in brain of AD patients, and seems to be implicated in the process of neuro-degeneration. A common polymorphism of the ICAM-1 gene (K469E) has been recently reported. In this case-control study, we evaluated the distribution of E/K alleles and genotypes of the ICAM-1 gene in 98 patients affected by sporadic AD and 115 age- and sex-matched controls. The frequency of the EE genotype was significantly higher in AD patients (P<0.01). Logistic regression analysis indicated that the presence of EE genotype significantly increased the risk of AD (odds ratio 3.01 [1.1-8.0], P<0.05). This study shows for the first time an association between ICAM-1 E/K gene polymorphism and AD, suggesting that polymorphisms of the ICAM-1 gene may be clinically important and confirming that inflammatory mechanisms may be crucial in the pathophysiology of neuro-degenerative diseases. PMID:12498973

Pola, Roberto; Flex, Andrea; Gaetani, Eleonora; Santoliquido, Angelo; Serricchio, Michele; Pola, Paolo; Bernabei, Roberto

67

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

68

Effect of thalidomide dithiocarbamate analogs on the intercellular adhesion molecule-1 expression.  

PubMed

Thalidomide has been reported to have anti-angiogenic and antimetastatic effects. Intercellular adhesion molecule-1 (ICAM-1) was shown to be involved in monocyte adherence to epithelial cells and cancer cell invasion. Novel thalidomide dithiocarbamate analogs (containing 2 sulfur atoms) were designed and synthesized as potential anti-tumor agents. The aim of this work is to investigate their anti-tumor effect against transplantable experimental tumor, Ehrlich ascites carcinoma (EAC), in mice by studying the changes in cell's biochemical profile, the expression of ICAM-1 and nitric oxide (NO) and their association with tumor burden. As shown in our results, treatment of solid tumor-bearing mice with thalidomide 1 resulted in a significant reduction in tumor volume with 75.4% inhibition, a significant decrease in lactate dehydrogenase (LDH), ICAM-1 expression and NO. Thalidomide dithiocarbamate analogs 2 and 3 exhibited a potent effect to reduce the volume of solid tumor with 96.7% and 96.5% inhibition, respectively, a significant ability to increase the albumin, alanine aminotransferase (ALT) and glucose levels and to diminish LDH, ICAM-1 expression and NO. Thalidomide dithiocarbamate analog 3 has more potent anti-tumor activity as compared with thalidomide 1 or its dithiocarbamate analog 2. Taken together, our study improved that the dithiocarbamate analogs 2 and 3 are more potent anti-tumor agents with more pronounced effect than thalidomide 1 itself. PMID:20438868

Guirgis, Adel A; Zahran, Magdy A H; Mohamed, Amr S; Talaat, Roba M; Abdou, Bishoy Y; Agwa, Hussein S

2010-05-09

69

Corticosteroids inhibit rhinovirus-induced intercellular adhesion molecule-1 up-regulation and promoter activation on respiratory epithelial cells  

Microsoft Academic Search

Background: Rhinoviruses are associated with the majority of asthma exacerbations. To date, the pathogenesis of virus-induced asthma exacerbations is still unclear, and no safe effective therapy is available. Intercellular adhesion molecule-1 (ICAM-1) has a central role in inflammatory cell recruitment to the airways in asthma and is the receptor for 90% of rhinoviruses. We have previously shown that rhinovirus infection

Alberto Papi; Nikolaos G. Papadopoulos; Klaus Degitz; Stephen T. Holgate; Sebastian L. Johnston

2000-01-01

70

The role of intercellular adhesion molecule 1 and neutrophils in acute pancreatitis and pancreatitis-associated lung injury  

Microsoft Academic Search

Background & Aims: Intercellular adhesion molecule 1 (ICAM-1) and neutrophils play important roles in many inflammatory processes, but their importance in both acute pancreatitis and pancreatitis-associated lung injury has not been defined. Methods: To address this issue, mice that do not express ICAM-1 were used and depleted of neutrophils by administration of antineutrophil serum. Pancreatitis was induced by administering either

Jean-Louis Frossard; Ashok Saluja; Lakshmi Bhagat; Hong Sik Lee; Madhav Bhatia; Bernd Hofbauer; Michael L. Steer

1999-01-01

71

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

72

Active site formation, not bond kinetics, limits adhesion rate between human neutrophils and immobilized vascular cell adhesion molecule 1.  

PubMed

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. PMID:19134479

Waugh, Richard E; Lomakina, Elena B

2009-01-01

73

Leukocytosis and resistance to septic shock in intercellular adhesion molecule 1-deficient mice  

PubMed Central

Intercellular adhesion molecule 1 (ICAM-1) is one of three immunoglobulin superfamily members that bind to the integrins lymphocyte function associated 1 (LFA-1) and Mac-1 on leukocytes. We have generated mice that are genetically and functionally deficient in ICAM-1. These mice have elevated numbers of circulating neutrophils and lymphocytes, as well as diminished allogeneic T cell responses and delayed type hypersensitivity. Mutant mice are resistant to lethal effects of high doses of endotoxin (lipopolysaccharide [LPS]), and this correlates with a significant decrease in neutrophil infiltration in the liver. Production of inflammatory cytokines such as tumor necrosis factor alpha or interleukin 1 is normal in ICAM-1-deficient mice, and thus protection appears to be related to a diminution in critical leukocyte-endothelial interactions. After sensitization with D- galactosamine (D-Gal), ICAM-1-deficient mice are resistant to the lethal effect of low doses of exotoxin (Staphylococcus aureus enterotoxin B [SEB]), which has been shown to mediate its toxic effects via the activation of specific T cells. In this model, ICAM-1-mediated protection against SEB lethality correlates with a decrease in the systemic release of inflammatory cytokines, as well as with prevention of extensive hepatocyte necrosis and hemorrhage. ICAM-1-deficient mice sensitized with D-Gal, however, are not protected from lethality when challenged with low doses of endotoxin (LPS). These studies show that the different contribution of ICAM-1 in the activation of either T cells or macrophages is decisive for the fatal outcome of the shock in these two models. This work suggests that anti-ICAM-1 therapy may be beneficial in both gram-positive and -negative septic shock, either by reducing T cell activation or by diminishing neutrophil infiltration.

1994-01-01

74

Junctional adhesion molecule 1 is a functional receptor for feline calicivirus.  

PubMed

The life cycle of calicivirus is not fully understood because most of the viruses cannot be propagated in tissue culture cells. We studied the mechanism of calicivirus entry into cells using feline calicivirus (FCV), a cultivable calicivirus. From the cDNA library of Crandell-Rees feline kidney (CRFK) cells, feline junctional adhesion molecule 1 (JAM-1), an immunoglobulin-like protein present in tight junctions, was identified as a cellular-binding molecule of the FCV F4 strain, a prototype strain in Japan. Feline JAM-1 expression in nonpermissive hamster lung cells led to binding and infection by F4 and all other strains tested. An anti-feline JAM-1 antibody reduced the binding of FCV to permissive CRFK cells and strongly suppressed the cytopathic effect (CPE) and FCV progeny production in infected cells. Some strains of FCV, such as F4 and F25, have the ability to replicate in Vero cells. We found that regardless of replication ability, FCV bound to Vero and 293T cells via simian and human JAM-1, respectively. In Vero cells, an anti-human JAM-1 antibody inhibited binding, CPE, and progeny production by F4 and F25. In addition, feline JAM-1 expression permitted FCV infection in 293T cells. Taken together, our results demonstrate that feline JAM-1 is a functional receptor for FCV, simian JAM-1 also functions as a receptor for some strains of FCV, and the interaction between FCV and JAM-1 molecules may be a determinant of viral tropism. This is the first report concerning a functional receptor for the viruses in the family Caliciviridae. PMID:16611908

Makino, Akiko; Shimojima, Masayuki; Miyazawa, Takayuki; Kato, Kentaro; Tohya, Yukinobu; Akashi, Hiroomi

2006-05-01

75

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

2013-05-21

76

Soluble intercellular adhesion molecule-1 (slCAM-1) for early diagnosis of neonatal infections.  

PubMed

We investigated the validity of circulating soluble intercellular adhesion molecule-1 (slCAM-1) as an early immunological marker of neonatal sepsis as compared to C-reactive protein (CRP), immature to total neutrophils ratio (IlT) and blood culture assays. The study included 28 full term neonates with clinical manifestations of sepsis, 10 of them had suspected sepsis "Group I" with negative blood culture, positive CRP during 1st week of life and one or more risk factors for infections. The other 18 neonates had proven sepsis "Group II"; with positive blood culture and positive CRP. 14 normal age and sex matched controls "Group III" were also included. Serum slCAM-1 concentrations (ng/ml) were measured using enzyme linked immunosorbent assay (ELISA) in two successive blood samples; before (S1) and one week after (S2) the start of antibiotics respectively. The mean value of I/T ratio was significantly higher in both SI and S2 (P<0.05; P<0.001 respectively) in septic neonates compared with controls. In addition, a significant difference (P<0.05) was detected in S2 between mean CRP levels in group I (9.6+/-15.7 mg/dl) and group II (17.3+/-30.0 mg/dl). The mean values of slCAM-1 in (Sl) of septic groups I and II (445.7+/-138.5 and 512.8+240.9 ng/ml respectively) were significantly higher (P<0.05) than those of control group (364.0+/-67.4). In contrast, in (S2) insignificant differences were detected between both groups (392.6+/-149.8 and 420.0+/-184.7 respectively) and controls. A positive correlation was revealed between CRP and slCAM-1 values in (Sl) (r=0.3, P<0.05). Positive correlations were also detected between slCAM-1 levels and leukocytic counts (r=0.3, P<0.05) and CRP (r=0.5, P<0.001) in (S2) while, negative correlation was detected between slCAM-1 levels and platelet counts (r= -0.5, P<0.001). In conclusion, serum concentration of ICAM-1 is a potential marker for diagnosis of neonatal sepsis at its early stages. PMID:22059356

Mahmoud, Samia; Maklad, Soheir; Abo Elmagd, Enas K

2009-01-01

77

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

78

The role of endothelial cell adhesion molecules P-selectin, E-selectin and intercellular adhesion molecule-1 in leucocyte recruitment induced by exogenous methylglyoxal  

PubMed Central

Methylglyoxal (MG) is a reactive dicarbonyl metabolite formed during glucose, protein and fatty acid metabolism. In hyperglycaemic conditions, increased MG level has been linked to the development of diabetes and its vascular complications at the macrovascular and microvascular levels where inflammation plays a role. To study the mechanism of MG-induced inflammation in vivo, we applied MG locally to healthy mice and used intravital microscopy to investigate the role of endothelial cell adhesion molecules in MG-induced leucocyte recruitment in cremasteric microvasculature. Administration of MG (25 and 50 mg/kg) to the tissue dose-dependently induced leucocyte recruitment at 4·0–5·5 hr, with 84–92% recruited cells being neutrophils. Such MG treatment up-regulated the expression of endothelial cell adhesion molecules P-selectin, E-selectin, intercellular adhesion molecule-1, but not vascular cell adhesion molecule-1. Activation of the nuclear factor-?B signalling pathway contributed to MG-induced up-regulation of these adhesion molecules and leucocyte recruitment. The role of the up-regulated endothelial cell adhesion molecules in MG-induced leucocyte recruitment was determined by applying specific functional blocking antibodies to MG-treated animals and observing changes in leucocyte recruitment parameters. Our data demonstrate that the up-regulation of P-selectin, E-selectin and intercellular adhesion molecule-1 contributes to the increased leucocyte rolling flux, reduced leucocyte rolling velocity, and increased leucocyte adhesion, respectively. Our results reveal the role of endothelial cell adhesion molecules in MG-induced leucocyte recruitment in microvasculature, an inflammatory condition related to diabetic vascular complications.

Su, Yang; Lei, Xi; Wu, Lingyun; Liu, Lixin

2012-01-01

79

Association between intercellular adhesion molecule-1 E\\/K gene polymorphism and probable vascular dementia in humans  

Microsoft Academic Search

Intercellular adhesion molecule-1 (ICAM-1) is implicated in the pathogenesis of ischemic cardiovascular disorders, including cerebral ischemia. A common polymorphism of the ICAM-1 gene (K469E) has been recently reported. In this case-control study, we evaluated the association between this polymorphism and vascular dementia (VD) by studying 107 patients affected by probable VD and 115 age- and sex-matched controls. The frequency of

Roberto Pola; Andrea Flex; Eleonora Gaetani; Pierangelo Papaleo; Demetrio De Martini; Laura Gerardino; Michele Serricchio; Paolo Pola; Roberto Bernabei

2002-01-01

80

Up-regulation of intercellular adhesion molecule 1 in cerebral microvessels after cortical contusion trauma in a rat model  

Microsoft Academic Search

A study was made on the expression of the intercellular adhesion molecule 1 (ICAM-1) in cerebral microvessels after cortical\\u000a contusion trauma of the rat brain. The trauma was produced by a free-falling weight on the exposed dura of one fronto-parietal\\u000a lobe. Immunohistochemistry was done on cryostat sections using a monoclonal antibody and the reaction product was visualized\\u000a using the avidin-biotin-peroxidase

Jonas Isaksson; Anders Lewén; Lars Hillered; Yngve Olsson

1997-01-01

81

Association between type 1 diabetes age-at-onset and intercellular adhesion molecule-1 (ICAM-1) gene polymorphism  

Microsoft Academic Search

We investigated the intercellular adhesion molecule-1 (ICAM-1) gene polymorphism in 90 patients with young-onset type 1 diabetes, 74 with adult-onset type 1 diabetes, and 171 control subjects. The distribution of C-T genotypes and allele frequencies in exon 6 of the ICAM-1 gene was significantly different between adult-onset type 1 diabetes patients and controls (?2 = 9.76, p = 0.0076), and

Masataka Nishimura; Hiroshi Obayashi; Etsuko Maruya; Mitsuhiro Ohta; Hisataka Tegoshi; Michiaki Fukui; Goji Hasegawa; Hirofumi Shigeta; Yoshihiro Kitagawa; Koji Nakano; Hiroh Saji; Naoto Nakamura

2000-01-01

82

[Soluble adhesion molecules in muscular dystrophy].  

PubMed

To determine whether soluble adhesion molecules are affected in muscular dystrophy, we measured serum levels of creatine kinase (CK), soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble intercellular adhesion molecule-1 (sICAM-1), soluble (s) E-selectin, and fibrin and fibrinogen degradation products (FDP) in 25 patients with Duchenne muscular dystrophy (DMD), 7 with Becker muscular dystrophy, 7 with Fukuyama type congenital muscular dystrophy, 6 with myotonic dystrophy (MyD), and 5 with spinal muscular atrophy (SMA) type 2, and also serum sVCAM-1, sICAM-1, and sE-selectin in 9 healthy controls. The levels of sVCAM-1 in the patients with DMD were 367.0-852.0 ng/ml (552.8 +/- 23.1) and significantly elevated than those in the patients with MyD, SMA type 2, and controls. The levels of sICAM-1 and sE-selectin in the patients with muscular dystrophy were 0.2-376.0 ng/ml and 17.9-119.0 ng/ml, respectively. They were also elevated than those in the patients with SMA type 2 and controls, but not significantly. The levels of sVCAM-1 and sE-selectin in the patients with DMD significantly correlated with age. There was no correlation between the levels of soluble adhesion molecules and those of CK or FDP in any groups. These changes of soluble adhesion molecules may reflect the process of muscle destruction and endothelial cell activation in muscular dystrophy. PMID:12134684

Saito, Toshio; Yamamoto, Yuko; Shinno, Susumu

2002-07-01

83

PPARa Activators Inhibit Cytokine-Induced Vascular Cell Adhesion Molecule1 Expression in Human Endothelial Cells  

Microsoft Academic Search

Background—Adhesion molecule expression on the endothelial cell (EC) surface is critical for leukocyte recruitment to atherosclerotic lesions. Better understanding of transcriptional regulation of adhesion molecules in ECs may provide important insight into plaque formation. Peroxisome proliferator-activated receptor-a (PPARa), a member of the nuclear receptor family, regulates gene expression in response to certain fatty acids and fibric acid derivatives. The present

Nikolaus Mar; Galina K. Sukhova; Tucker Collins; Peter Libby; Jorge Plutzky

84

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

85

Intercellular Adhesion Molecule 1-Dependent Activation of Interleukin 8 Expression in Candida albicans-Infected Human Gingival Epithelial Cells  

PubMed Central

Increased induction of interleukin 8 (IL-8) and intercellular adhesion molecule 1 (ICAM-1) by oral epithelial cells may play a role in the host defense mechanism in oropharyngeal candidiasis; however, little is known about the expression feature of these molecules on human gingival epithelial cells (HGECs) during Candida albicans infection. In this report we present evidence that neutralization with antibody against ICAM-1 inhibited both the adherence of C. albicans to HGECs and the Candida-induced production of IL-8, suggesting a role for ICAM-1 in recognition and signaling in HGECs to express IL-8 upon infection with C. albicans.

Egusa, Hiroshi; Nikawa, Hiroki; Makihira, Seicho; Jewett, Anahid; Yatani, Hirofumi; Hamada, Taizo

2005-01-01

86

Intercellular adhesion molecule 1-dependent activation of interleukin 8 expression in Candida albicans-infected human gingival epithelial cells.  

PubMed

Increased induction of interleukin 8 (IL-8) and intercellular adhesion molecule 1 (ICAM-1) by oral epithelial cells may play a role in the host defense mechanism in oropharyngeal candidiasis; however, little is known about the expression feature of these molecules on human gingival epithelial cells (HGECs) during Candida albicans infection. In this report we present evidence that neutralization with antibody against ICAM-1 inhibited both the adherence of C. albicans to HGECs and the Candida-induced production of IL-8, suggesting a role for ICAM-1 in recognition and signaling in HGECs to express IL-8 upon infection with C. albicans. PMID:15618204

Egusa, Hiroshi; Nikawa, Hiroki; Makihira, Seicho; Jewett, Anahid; Yatani, Hirofumi; Hamada, Taizo

2005-01-01

87

Prevention of a chronic progressive form of experimental autoimmune encephalomyelitis by an antibody against mucosal addressin cell adhesion molecule-1, given early in the course of disease progression  

Microsoft Academic Search

A role for ?4 and ?7 integrins in mediating leucocyte entry into the central nervous system in the multiple sclerosis (MS)-like disease experimental autoimmune encephalomyelitis (EAE) has been demonstrated. However, the individual contributions of their respective ligands mucosal addressin cell adhesion molecule-1 (MAdCAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-cadherin expressed on the blood–brain barrier has not been determined. In

Jagat R Kanwar; Rupinder K Kanwar; Dongmao Wang; Geoffrey W Krissansen

2000-01-01

88

Experimental cerebral malaria develops independently of endothelial expression of intercellular adhesion molecule-1 (icam-1).  

PubMed

Cerebral malaria (CM) is a severe clinical complication of Plasmodium falciparum malaria infection and is characterized by a high fatality rate and neurological damage. Sequestration of parasite-infected red blood cells in brain microvasculature utilizes host- and parasite-derived adhesion molecules and is an important factor in the development of CM. ICAM-1, an alternatively spliced adhesion molecule, is believed to be critical on endothelial cells for infected red blood cell sequestration in CM. Using ICAM-1 mutant mice, we found that the full-length ICAM-1 isoform is not required for development of murine experimental CM (ECM) and that ECM phenotype varies with the combination of ICAM-1 isoforms expressed. Furthermore, we observed development of ECM in transgenic mice expressing ICAM-1 only on leukocytes, indicating that endothelial cell expression of this adhesion molecule is not required for disease pathogenesis. We propose that ICAM-1-dependent cellular aggregation, independent of ICAM-1 expression on the cerebral microvasculature, contributes to ECM. PMID:23493396

Ramos, Theresa N; Bullard, Daniel C; Darley, Meghan M; McDonald, Kristin; Crawford, David F; Barnum, Scott R

2013-03-14

89

The CCL2/CCR2 Axis Enhances Vascular Cell Adhesion Molecule-1 Expression in Human Synovial Fibroblasts  

PubMed Central

Background Chemokine ligand 2 (CCL2), also known as monocyte chemoattractant protein-1 (MCP-1), belongs to the CC chemokine family that is associated with the disease status and outcomes of osteoarthritis (OA). Here, we investigated the intracellular signaling pathways involved in CCL2-induced vascular cell adhesion molecule-1 (VCAM-1) expression in human OA synovial fibroblasts (OASFs). Methodology/Principal Findings Stimulation of OASFs with CCL2 induced VCAM-1 expression. CCL2-mediated VCAM-1 expression was attenuated by CCR2 inhibitor (RS102895), PKC? inhibitor (rottlerin), p38MAPK inhibitor (SB203580), and AP-1 inhibitors (curcumin and tanshinone IIA). Stimulation of cells with CCL2 increased PKC? and p38MAPK activation. Treatment of OASFs with CCL2 also increased the c-Jun phosphorylation and c-Jun binding to the AP-1 element on the VCAM-1 promoter. Moreover, CCL2-mediated CCR2, PKC?, p38MAPK, and AP-1 pathway promoted the adhesion of monocytes to the OASFs monolayer. Conclusions/Significance Our results suggest that CCL2 increases VCAM-1 expression in human OASFs via the CCR2, PKC?, p38MAPK, c-Jun, and AP-1 signaling pathway. The CCL2-induced VCAM-1 expression promoted monocytes adhesion to human OASFs.

Lin, Yu-Min; Hsu, Chin-Jung; Liao, Yuan-Ya; Chou, Ming-Chih; Tang, Chih-Hsin

2012-01-01

90

Tumor-derived intercellular adhesion molecule-1 mediates tumor-associated leukocyte infiltration in orthotopic pancreatic xenografts.  

PubMed

Tumor infiltration of immune cells (polymorphonuclear cells [PMNs] and macrophages) was initially thought to be an attempt by the host organism to combat malignancy. It appears, however, that certain subsets of chronically activated immune cells likely promote tumor growth, facilitate tumor cell survival and aid in metastasis. The association between tumor cells and tumor-associated PMNs has been demonstrated in several types of cancer, but the presence of tumor-associated PMNs in pancreatic cancer has not been well studied in vivo. Intercellular adhesion molecule-1 (ICAM-1) functions in cell-cell and cell-extracellular matrix adhesion and has a physiological role in PMN tight adhesion of leukocytes via interaction with the ligands LFA-1 and Mac-1. Increased ICAM-1 expression correlates with poor prognosis in pancreatic cancer. Therefore, the aim of this study was to investigate the function of ICAM-1 and tumor-associated PMNs in pancreatic cancer progression using ICAM-1-null (ICAM-1(-/-)) mice. We hypothesize that ICAM-1 null mice have decreased pancreatic cancer progression. Surprisingly, there is no significant difference in pancreatic cancer progression in wild-type versus ICAM-1 null mice. Interestingly, we found that tumor-derived ICAM-1 co-localizes with host PMNs at the leading edge of the tumor in ICAM-1 null mice. These results suggest that tumor-derived ICAM-1 is a sufficient ligand for tumor-associated PMNs and may play a role in subsequent tumor growth and metastasis. PMID:20404043

Roland, Christina L; Dineen, Sean P; Toombs, Jason E; Carbon, Juliet G; Smith, C Wayne; Brekken, Rolf A; Barnett, Carlton C

2010-02-01

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

Association between intercellular adhesion molecule-1 E/K gene polymorphism and probable vascular dementia in humans.  

PubMed

Intercellular adhesion molecule-1 (ICAM-1) is implicated in the pathogenesis of ischemic cardiovascular disorders, including cerebral ischemia. A common polymorphism of the ICAM-1 gene (K469E) has been recently reported. In this case-control study, we evaluated the association between this polymorphism and vascular dementia (VD) by studying 107 patients affected by probable VD and 115 age- and sex-matched controls. The frequency of the EE genotype was significantly higher in VD patients than controls (P=0.009). Logistic regression analysis indicated that the presence of the EE genotype significantly increased the risk of VD (odds ratio 3.25, P=0.024). Our findings support the hypothesis that ICAM-1 plays a role in the physiopathology of ischemic cerebrovascular disorders and suggest that genetic polymorphisms of ICAM-1 might be clinically important in the development and progression of neurodegenerative diseases. PMID:12095649

Pola, Roberto; Flex, Andrea; Gaetani, Eleonora; Papaleo, Pierangelo; De Martini, Demetrio; Gerardino, Laura; Serricchio, Michele; Pola, Paolo; Bernabei, Roberto

2002-07-01

93

De novo expression of intercellular adhesion molecule 1 (ICAM-1, CD54) in pancreas cancer.  

PubMed

We examined the expression of intercellular--adhesion molecule-I (ICAM-I, CD54) in 6 surgically removed pancreatic tumors and 8 pancreatic tumor cell lines. Immunohistochemistry revealed a varying percentage of ICAM-I-positive pancreas tumor cells, while normal pancreatic tissue (except for slight reactivity of endothelial cells) was not stained. The presence of the ICAM-I molecule on the cell surface and the expression of ICAM-I mRNA were investigated for 8 different pancreatic tumor cell lines. Three of these (Capan-I, Capan-2, QGP-I) expressed ICAM-I constitutively. In 4 of the ICAM-I-negative pancreas cancer cell lines, it was possible to induce a remarkable expression of ICAM-I by incubating the cells in the presence of inflammatory cytokines, whereas one cell line, 818-4, remained ICAM-I-negative. The responsiveness to either IFN-gamma, TNF-alpha, or IL-I beta treatment was shown to vary from cell line to cell line, indicating complex mechanisms that regulate the expression of ICAM-I at both, the transcriptional and the post-transcriptional level. Interestingly, ICAM-I is shed by pancreatic tumor cells, since soluble sICAM-I was detected in the cell-culture supernatants. In comparison with normal sera, the mean level of sICAM-I in sera of patients with pancreas carcinoma is elevated 2-fold. PMID:8093883

Schwaeble, W; Kerlin, M; Meyer zum Büschenfelde, K H; Dippold, W

1993-01-21

94

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

95

Expression of vascular cell adhesion molecule-1 (VCAM-1) by human brain microvessel endothelial cells in primary culture.  

PubMed

Vascular cell adhesion molecule-1 (VCAM-1) is an endothelial cell membrane glycoprotein that has been implicated in leukocyte/endothelial cell interactions in inflammation. In this study, we report the expression of VCAM-1 in primary cultures of human brain microvessel endothelial cells (HBMEC) under standard conditions and following bacterial lipopolysaccharide (LPS), tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), or interferon-gamma (IFN-gamma) treatment. Surface expression was detected and quantitated by light and immunogold electron microscopy and ELISA. Unstimulated cerebral endothelial cells (EC) constitutively expressed low levels of VCAM-1. LPS, TNF-alpha, or IL-1 beta increased the overall intensity of surface staining and the percentage of cells expressing VCAM-1 in a time- and concentration-dependent manner. LPS had the most potent effect, followed by TNF-alpha and then IL-1 beta. IFN-gamma did not upregulate VCAM-1. The level of VCAM-1 expression increased by 12-24 hr and returned to unstimulated levels by 48 hr. Immunoelectron microscopy demonstrated that VCAM-1 was preferentially localized on the apical as compared to the basal surface in both unstimulated and cytokine-treated cells. In addition, the intensity of immunostaining was significantly greater in stimulated versus unstimulated EC. The polarization and significant upregulation of VCAM-1 after cytokine treatment suggest a possible role of this adhesion molecule in inflammatory and autoimmune processes within the central nervous system. PMID:7543972

Wong, D; Dorovini-Zis, K

1995-05-01

96

MicroRNA-221 controls expression of intercellular adhesion molecule-1 in epithelial cells in response to Cryptosporidium parvum infection  

PubMed Central

Cryptosporidium parvum is a protozoan parasite that infects gastrointestinal epithelial cells and causes diarrheal disease in humans and animals globally. Pathological changes following C. parvum infection include crypt hyperplasia, a modest inflammatory reaction with increased infiltration of lymphocytes into intestinal mucosa. Expression of adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1), on infected epithelial cell surfaces may facilitate adhesion and recognition of lymphocytes at infection sites. MicroRNAs (miRNAs) are small RNA molecules of 23 nucleotides that negatively regulate protein-coding gene expression via translational suppression or mRNA degradation. We recently reported that microRNA-221 (miR-221) regulates ICAM-1 translation through targeting the ICAM-1 3?-untranslated region (UTR). In this study, we tested the role of miR-221 in regulating ICAM-1 expression in epithelial cells in response to C. parvum infection using an in vitro model of human biliary cryptosporidiosis. Up-regulation of ICAM-1 at both message and protein levels was detected in epithelial cells following C. parvum infection. Inhibition of ICAM-1 transcription with actinomycin D could only partially block C. parvum-induced ICAM-1 expression at the protein level. Cryptosporidium parvum infection decreased miR-221 expression in infected epithelial cells. When cells were transfected with a luciferase reporter construct covering the miR-221 binding site in the ICAM-1 3?-UTR and then exposed to C. parvum, an enhanced luciferase activity was detected. Transfection of miR-221 precursor abolished C. parvum-stimulated ICAM-1 protein expression. In addition, expression of ICAM-1 on infected epithelial cells facilitated epithelial adherence of co-cultured Jurkat cells. These results indicate that miR-221-mediated translational suppression controls ICAM-1 expression in epithelial cells in response to C. parvum infection.

Gong, Ai-Yu; Hu, Guoku; Zhou, Rui; Liu, Jun; Feng, Yaoyu; Soukup, Garrett A.; Chen, Xian-Ming

2011-01-01

97

A randomized, double-blind trial of the effect of treatment with montelukast on bronchial hyperresponsiveness and serum eosinophilic cationic protein (ECP), soluble interleukin 2 receptor (sIL2R), IL4, and soluble intercellular adhesion molecule 1 (sICAM-1) in children with asthma  

Microsoft Academic Search

Background: Anti-inflammatory properties of leukotriene modifiers and their effect on bronchial hyperresponsiveness have not been studied in children with asthma. Objective: The primary objective of this study was to determine the changes in serum levels of inflammatory mediators, clinical efficacy, and bronchial hyperresponsiveness after treatment with montelukast. Methods: In this double-blind, randomized, placebo-controlled trial, 39 children with mild-to-moderate atopic asthma

Iwona Stelmach; Joanna Jerzynska; Piotr Kuna

2002-01-01

98

Is the intercellular adhesion molecule-1/leukocyte function associated antigen 1 pathway of leukocyte adhesion involved in the tissue damage of alcoholic hepatitis?  

PubMed Central

Alcoholic hepatitis is characterised histologically by an intense inflammatory cell infiltrate made up predominantly of neutrophils but including other cell types, particularly lymphocytes. Leukocyte cytotoxicity requires cell adhesion, which is mediated via receptors on the leukocyte surface including leukocyte function associated antigen-1 (LFA-1) which binds to the ligand intercellular adhesion molecule-1 (ICAM-1) on the target cell. The distribution of ICAM-1 and LFA-1 expression in liver biopsy specimens from patients with alcoholic liver disease was examined to ascertain whether this pathway of leukocyte adhesion is involved in the tissue damage of alcoholic hepatitis. Specimens were stained for ICAM-1 and LFA-1 by a three step immunoalkaline-phosphatase method using monoclonal antibodies against ICAM-1 and LFA-1. LFA-1 staining on portal tract inflammatory cells and parenchymal inflammatory cells and ICAM-1 staining on liver components were examined. ICAM-1 expression on hepatocytes was significantly greater in alcoholic hepatitis compared with fatty liver (p less than 0.001) and normal controls (p less than 0.01). ICAM-1 expression correlated with the histological degree of hepatocellular damage (tau = 0.79; p = 0.0005) and parenchymal inflammation (tau = 0.65; p less than 0.001, and with LFA-1 expression on parenchymal leukocytes (tau = 0.63; p = 0.01). The ICAM-1/LFA-1 pathway may therefore be involved in leukocyte mediated tissue damage during alcoholic hepatitis. Images Figure 2 Figure 3 Figure 4

Burra, P; Hubscher, S G; Shaw, J; Elias, E; Adams, D H

1992-01-01

99

Suppressive effect of short-interfering RNA on hyperglycemia-induced expression of intercellular adhesion molecule-1 on cultured vascular endothelial cells  

Microsoft Academic Search

Purpose  The pathology of diabetic retinopathy involves endothelial dysfunction, in which leukocyte adhesion to the vascular endothelium\\u000a via intercellular adhesion molecule-1 (ICAM-1) may play a key role. Short-interfering RNAs (siRNAs) are unique modulators\\u000a of gene expression in mammalian cells. The purpose of this study was to evaluate the enhanced effect of hyperglycemia and\\u000a the attenuating effect of siRNAs on ICAM-1 expression

Ayae Takase; Tsutomu Yasukawa; Aki Kato; Yuichiro Ogura

2008-01-01

100

Interleukin8 and Intercellular Adhesion Molecule 1 Regulation in Oral Epithelial Cells by Selected Periodontal Bacteria: Multiple Effects of Porphyromonas gingivalis via Antagonistic Mechanisms  

Microsoft Academic Search

Interaction of bacteria with mucosal surfaces can modulate the production of proinflammatory cytokines and adhesion molecules produced by epithelial cells. Previously, we showed that expression of interleukin-8 (IL-8) and intercellular adhesion molecule 1 (ICAM-1) by gingival epithelial cells increases following inter- action with several putative periodontal pathogens. In contrast, expression of IL-8 and ICAM-1 is reduced after Porphyromonas gingivalis ATCC

GEORGE T.-J. HUANG; DANIEL KIM; JONATHAN K.-H. LEE; HOWARD K. KURAMITSU; SUSAN KINDER HAAKE

2001-01-01

101

Inflammation-specific T1 imaging using anti-intercellular adhesion molecule 1 antibody-conjugated gadolinium diethylenetriaminepentaacetic acid.  

PubMed

To examine inflammatory tissue, an initial and common symptom of various types of pathogenesis, we designed inflammation-targeted T(1) contrast agents prepared by bioconjugation of gadolinium diethylenetriaminepentaacetic acid (Gd-DTPA) with anti-intercellular adhesion molecule 1 (ICAM-1) antibody. The anti-ICAM-1 antibody was coupled with DTPA and was then conjugated with Gd. The specific binding of the Gd-DTPA-anti-ICAM-1 antibody complex to the ICAM-1-expressing cells was examined in the cultured endothelial cells where ICAM-1 expression was stimulated. Inflammation-specific T(1) imaging was then assessed using a mouse abscess model with the 1.5-Tesla module. The Gd-DTPA-anti-ICAM-1 antibody displayed increased r1, which was two times higher than that of Gd-DTPA and showed predominant binding to cultured endothelial cells, which expressed a high level of ICAM-1. Moreover, the inflammation-specific T(1) enhancement was imaged with the Gd-DTPA-anti-ICAM-1 antibody in the mouse acute inflammation model. The Gd-DTPA-anti-ICAM-1 antibody showed significantly increased vascular circulation time, which thereby offered a greater chance for its binding to the target cells. The Gd-DTPA-anti-ICAM-1 antibody displays a potential targeted T(1) contrast agent specific to the inflammatory tissue that expresses ICAM-1. PMID:17445502

Choi, Kyu-Sil; Kim, Sun-Hee; Cai, Quan-Yu; Kim, Soo-Yeon; Kim, Hyang-Ok; Lee, Hye-Jin; Kim, Eun-A; Yoon, Seong-Eon; Yun, Ki-Jung; Yoon, Kwon-Ha

102

Soluble CD14 mediates lipopolysaccharide-induced intercellular adhesion molecule 1 expression in cultured human gingival fibroblasts.  

PubMed Central

Intercellular adhesion molecule 1 (ICAM-1) is involved in the accumulation and activation of leukocytes in inflammatory diseases such as periodontitis. As reported previously, ICAM-1 is up-regulated on cultured human gingival fibroblasts (HGF) by exposure to lipopolysaccharide (LPS), suggesting a specific LPS recognition mechanism. We therefore investigated the role of CD14, an LPS receptor, in stimulation of HGF by LPS. Cell surface CD14 antigen was not observed on HGF by flow cytometric analysis. In addition, expression of CD14 mRNA in HGF was not detected by reverse transcription-PCR analysis. Since HGF did not express endogenous CD14, we investigated the role of human serum-derived soluble CD14 (sCD14) in ICAM-1 induction on HGF by LPS. The serum-dependent ICAM-1 induction by LPS was observed in HGF. In medium containing human serum, anti-CD14 antibody inhibited ICAM-1 induction on HGF by LPS. Depletion of sCD14 from human serum markedly reduced ICAM-1 expression on HGF in response to LPS. Supplementation of the serum-free medium with sCD14 alone restored the capacity of HGF to respond to LPS. These results show that induction of ICAM-1 in HGF by LPS does not involve binding to cell surface CD14 but is mediated by serum-derived sCD14.

Hayashi, J; Masaka, T; Saito, I; Ishikawa, I

1996-01-01

103

Effects of cytokines and periodontopathic bacteria on the leukocyte function-associated antigen 1/intercellular adhesion molecule 1 pathway in gingival fibroblasts in adult periodontitis.  

PubMed Central

We investigated the effects of inflammatory cytokines and periodontopathic bacteria on expression of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1, and E-selectin (endothelial leukocyte adhesion molecule 1) in cultured human gingival fibroblasts (HGF). Cell surface ICAM-1 was upregulated on HGF under transcriptional control by exposure not only to interleukin-1 beta, tumor necrosis factor alpha, and gamma interferon but also to sonic extracts prepared from Porphyromonas gingivalis and Prevotella intermedia (nigrescens) and lipopolysaccharides from Escherichia coli. However, these stimuli induced only minimal expression of vascular cell adhesion molecule 1 and E-selectin on HGF. Binding assays using HGF and Molt 4, the human T-cell leukemia cell line, showed induced ICAM-1 to be functional, and the increased binding was blocked by a combination of monoclonal antibodies against ICAM-1 and leukocyte function-associated antigen 1. Furthermore, gingival tissues from adult periodontitis patients showed increased mRNA expression of ICAM-1 compared with that in tissues from normal healthy donors. In immunohistological analysis, we also observed in vivo that the expression of ICAM-1 on fibroblasts in adult periodontitis tissues was greater than that in normal gingiva. Thus, the overexpression of ICAM-1 on gingival fibroblasts induced by cytokines and periodontopathic bacteria is speculated to be deeply involved in the accumulation and retention of leukocyte function-associated antigen 1-bearing leukocytes in adult periodontitis lesions. Images

Hayashi, J; Saito, I; Ishikawa, I; Miyasaka, N

1994-01-01

104

Effect of desloratadine and loratadine on rhinovirus-induced intercellular adhesion molecule 1 upregulation and promoter activation in respiratory epithelial cells  

Microsoft Academic Search

Background: Rhinoviruses have been recently associated with the majority of asthma exacerbations for which current therapy is inadequate. Intercellular adhesion molecule 1 (ICAM-1) has a central role in airway inflammation in asthma, and it is the receptor for 90% of rhinoviruses. Rhinovirus infection of airway epithelium induces ICAM-1. Desloratadine and loratadine are compounds belonging to the new class of H1-receptor

Alberto Papi; Nikolaos G. Papadopoulos; Luminita A. Stanciu; Klaus Degitz; Stephen T. Holgate; Sebastian L. Johnston

2001-01-01

105

The Cutaneous Lymphocyte Antigen Is a Skirt Lymphocyte Homing Receptor for the Vascular Lectin Endothelial Cell-Leukocyte Adhesion Molecule 1  

Microsoft Academic Search

Summary A skin-associated population of memory T lymphocytes, defined by expression of the cutaneous lymphocyte antigen (CLA), binds selectively and avidly to the vascular lectin endothelial cell- leukocyte adhesion molecule 1 (ELAM-1), an interaction that may be involved in targeting of CLA + T cells to cutaneous sites of chronic inflammation. Here we present evidence that CLA itself is the

Martyn K. Robinson; R. Aaron Warnock; Takashi K. Kishimoto; Louis J. Picker; Eugene C. Butcher

106

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

107

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

2013-07-27

108

Pentoxifylline inhibits intercellular adhesion molecule-1 (ICAM-1) and lung injury in experimental phosgene-exposure rats.  

PubMed

Phosgene inhalation results in acute lung injury (ALI) mostly, pulmonary edema and even acute respiratory distress syndrome, but there is no specific antidote. Inflammatory cells play an important role in the ALI caused by phosgene. Intercellular adhesion molecule-1 (ICAM-1) is a critical factor for inflammatory organ injury. We hypothesized that pentoxifylline (PTX), an inhibitor of leukocyte activation, would have a protective effect on experimental phosgene-induced lung injury rats by inhibiting ICAM-1. To prove this hypothesis, we used rat models of phosgene (400 ppm x 1 min)-induced injury to investigate: (1) the time course of lung injury (control 1, 3, 6, 12, 24, and 48 h group), including pathological changes in hematoxylin and eosin staining and transmission electron microscope, myeloperoxidase (MPO) activity by colorimetric method and ICAM-1 protein level detected by western blot, (2) At 3 h after phosgene exposure, protective effects of different dosages of PTX (50 mg/kg and 100 mg/kg) administration were evaluated by MPO activity, ICAM-1 differential expression and WBC count in bronchoalveolar lavage fluid. The results showed that inflammatory cells emerged out of lung blood vessels at 3 h after phosgene exposure. The MPO activity of lung tissue increased significantly from 3 to 48 h after phosgene exposure (P < 0.05) and ICAM-1 expression presented a similar change, especially at 3 h and 24 h (P < 0.05). After pretreatment and treatment with PTX (100 mg/kg), significant protective effects were shown (P < 0.05). These data supported our hypothesis that PTX reduced phosgene-induced lung injury, possibly by inhibiting ICAM-1 differential expression. PMID:20569121

Zhang, Xiao-di; Hou, Jun-Feng; Qin, Xu-Jun; Li, Wen-Li; Chen, Hong-Li; Liu, Rui; Liang, Xin; Hai, Chun-Xu

2010-09-01

109

Microparticle-associated vascular adhesion molecule-1 and tissue factor follow a circadian rhythm in healthy human subjects.  

PubMed

An increased risk of death or severe injury due to late-morning thrombotic events is well established. Tissue factor (TF) is the initiator of the coagulation cascade, and endothelial stresses, coupled with production of pro-coagulant microparticles (MP) are also important factors in loss of haemostasis. TF and vascular cell adhesion molecule-1 (VCAM-1) -positive cell microparticles were assessed periodically over a 24-hour (h) period in healthy human subjects to ascertain if they followed a circadian rhythm. Eleven healthy male subjects were assessed in a temperature-controlled environment with dietary intake consistent between subjects. Blood samples were taken every 4 h by venipuncture, and TF and VCAM-1 positive microparticles were quantified by flow cytometry. A significant circadian rhythm was observed in VCAM-1 MP (p=or<0.0001), and a trend was shown, although not statistically significant (p=0.065) in TF microparticles. A peak was observed at 9 a.m. for VCAM-1 positive MP, followed by a decrease and subsequent peak at 9 p.m. and a minimum at 5 a.m. TF-positive MP followed a strikingly similar trend in both variation and absolute numbers with a delay. A circadian rhythm was observed in VCAM-1 and less so TF-positive MP. This has significant implications in terms of the well known increased risk of cardiovascular thrombotic events matching this data. To our knowledge this is the first such report of quantified measurements of these MP over a 24-h period and the only measurement of a 24-h variation of in-vivo blood-borne TF. PMID:18449421

Madden, Leigh A; Vince, Rebecca V; Sandström, Marie E; Taylor, Lee; McNaughton, Lars; Laden, Gerard

2008-05-01

110

Endogenous prostaglandin D(2) synthesis decreases vascular cell adhesion molecule-1 expression in human umbilical vein endothelial cells.  

PubMed

We examined the role of prostaglandin D(2) (PGD(2)) in the expression of vascular cell adhesion molecule-1 (VCAM)-1 following interleukin-1beta (IL-1) stimulation in human umbilical vein endothelial cells (HUVEC) transfected with lipocaline-type PGD(2) synthase (L-PGDS) genes. HUVEC were isolated from human umbilical vein and incubated with 20 U/ml IL-1 and various concentrations of authentic PGD(2). The isolated HUVEC were also transfected with L-PGDS genes by electroporation. The L-PGDS-transfected HUVEC were used to investigate the role of endogenous PGD(2) in IL-1-stimulated VCAM-1 biosynthesis. We also used an anti-PGD(2) antibody to examine whether an intracrine mechanism was involved in VCAM-1 production. PGD(2) and VCAM-1 levels were determined by radio- and cell surface enzyme-immunoassay, respectively. VCAM-1 mRNA was assessed by RT-PCR. IL-1-stimulated VCAM-1 expression by HUVEC was dose-dependently inhibited by authentic PGD(2). L-PGDS gene-transfected HUVEC produced more PGD(2) than HUVEC transfected with the reporter gene alone. IL-1 induced increases in VCAM-1 expression in HUVEC transfected with reporter genes alone. However, this effect was significantly attenuated in the case of IL-1 stimulation of HUVEC transfected with L-PGDS genes, and accompanied by an apparent suppression of VCAM-1 mRNA expression. Neutralization of extracellular PGD(2) by anti-PGD(2)-specific antibody influenced neither VCAM-1 mRNA expression nor VCAM-1 biosynthesis. In conclusion, HUVEC transfected with L-PGDS genes showed increased PGD(2) synthesis. This increase was associated with attenuation of both VCAM-1 expression and VCAM-1 mRNA expression. The results suggest that endogenous PGD(2) decreases VCAM-1 expression and VCAM-1 mRNA expression, probably through an intracrine mechanism. PMID:16154157

Negoro, Hideyuki; Shin, Wee Soo; Hakamada-Taguchi, Rie; Eguchi, Naomi; Urade, Yoshihiro; Goto, Atsuo; Toyo-Oka, Teruhiko; Fujita, Toshiro; Omata, Masao; Uehara, Yoshio

2005-09-08

111

Serum inter-cellular adhesion molecule 1 is an early marker of diagnosis and prediction of severe acute pancreatitis  

PubMed Central

AIM: To determine if serum inter-cellular adhesion molecule 1 (ICAM-1) is an early marker of the diagnosis and prediction of severe acute pancreatitis (SAP) within 24 h of onset of pain, and to compare the sensitivity, specificity and prognostic value of this test with those of acute physiology and chronic health evaluation (APACHE)?II?score and interleukin-6 (IL-6). METHODS: Patients with acute pancreatitis (AP) were divided into two groups according to the Ranson’s criteria: mild acute pancreatitis (MAP) group and SAP group. Serum ICAM-1, APACHE?IIand IL-6 levels were detected in all the patients. The sensitivity, specificity and prognostic value of the ICAM-1, APACHE?IIscore and IL-6 were evaluated. RESULTS: The ICAM-1 level in 36 patients with SAP within 24 h of onset of pain was increased and was significantly higher than that in the 50 patients with MAP and the 15 healthy volunteers (P < 0.01). The ICAM-1 level (25 ng/mL) was chosen as the optimum cutoff to distinguish SAP from MAP, and the sensitivity, specificity, positive predictive value, negative predictive value (NPV), positive likelihood ratio and negative likelihood ratio were 61.11%, 71.42%, 0.6111, 0.7142, 2.1382 and 0.5445, respectively. The area under the curve demonstrated that the prognostic accuracy of ICAM-1 (0.712) was similar to the APACHE-IIscoring system (0.770) and superior to IL-6 (0.508) in distinguishing SAP from MAP. CONCLUSION: ICAM-1 test is a simple, rapid and reliable method in clinical practice. It is an early marker of diagnosis and prediction of SAP within the first 24 h after onset of pain or on admission. As it has a relatively low NPV and does not allow it to be a stand-alone test for the diagnosis of AP, other conventional diagnostic tests are required.

Zhu, Hai-Hang; Jiang, Lin-Lin

2012-01-01

112

Functional Implication of the Hydrolysis of Platelet Endothelial Cell Adhesion Molecule 1 (CD31) by Gingipains of Porphyromonas gingivalis for the Pathology of Periodontal Disease  

PubMed Central

Periodontitis is a response of highly vascularized tissues to the adjacent microflora of dental plaque. Progressive disease has been related to consortia of anaerobic bacteria, with the gram-negative organism Porphyromonas gingivalis particularly implicated. The gingipains, comprising a group of cysteine proteinases and associated hemagglutinin domains, are major virulence determinants of this organism. As vascular expression of leukocyte adhesion molecules is a critical determinant of tissue response to microbial challenge, the objective of this study was to determine the capacity of gingipains to modulate the expression and function of these receptors. Given the potential multifunctional role of platelet endothelial cell adhesion molecule 1 (PECAM-1) in the vasculature, the effect of gingipains on PECAM-1 expression by endothelial cells was examined. Activated gingipains preferentially down-regulated PECAM-1 expression on endothelial cells compared with vascular cell adhesion molecule 1 and endothelial-leukocyte adhesion molecule 1, but the reduction in PECAM-1 expression was completely inhibited in the presence of the cysteine proteinase inhibitor TLCK (N?-p-tosyl-l-lysine chloromethyl ketone). Endothelial monolayers treated with activated gingipains demonstrated progressive intercellular gap formation that correlated with reduced intercellular junctional PECAM-1 expression as determined by Western blotting and immunofluorescence microscopy. This was accompanied by enhanced transfer of both albumin and neutrophils across the monolayer. The results suggest that degradation of PECAM-1 by gingipains contributes to increased vascular permeability and neutrophil flux at disease sites.

Yun, Peter L. W.; Decarlo, Arthur A.; Chapple, Cheryl C.; Hunter, Neil

2005-01-01

113

Adhesion molecule levels in serum and cerebrospinal fluid in children with bacterial meningitis and sepsis  

PubMed Central

Background: Adhesion molecules play a role in leukocyte recruitment during central nervous system (CNS) inflammation. Aim: This study was designed to compare serum, cerebrospinal fluid (CSF) concentrations of adhesion molecules in children with meningitis and sepsis, and to evaluate their sources. Setting: This study was carried out at Pediatric Department, King Abdulaziz University Hospital from January 2007 to June 2008. Design: Serum and CSF samples were collected on admission from meningitis (n = 40), sepsis (n = 20) patients, and sera from controls (n = 20). Materials and Methods: Endothelial (E), leukocyte (L), platelet (P) selectins intercellular cell adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecules-1 (VCAM-1) were measured using ELISA. Statistics: ANOVA and Spearman's correlations were used. Adhesion molecules with albumin concentration were estimated in CSF/serum to calculate concentration quotients. Results: In meningitis, serum sE-, sL-, sP-selectins sICAM-1, sVCAM-1 levels were higher than controls. Compared to sepsis, serum sE-selectin, sL-selectin, sVCAM-1, CSF-sL-selectin, CSF-sVCAM-1, VCAM-1 ratio and index were higher, while serum sP-selectin was lower than meningitis. sE-selectin ratio, CSF sICAM-1 were higher in meningitis with positive than negative culture. The sE-selectin index was higher in meningitis with neurological complication than those without it. In meningitis, correlation was found between CSF protein and CSF white blood cell counts (WBCs), CSF sICAM-1, CSF sVCAM-1 and between CSF sE-selectin and CSF sICAM-1. Conclusions: This study supports the role of adhesion molecules especially sL-selectin, sVCAM-1 in meningitis and suggests further research to determine their use as biomarkers for meningitis and use of their antagonists as therapeutic for CNS inflammation. The presence of discrepancy of CSF/serum ratios for molecules of same molecular weight suggest intrathecal shedding in addition to diffusion through the blood-CSF barrier.

Jaber, Soad M.; Hamed, Enas A.; Hamed, Sherifa A.

2009-01-01

114

Soluble adhesion molecules and myocardial injury during coronary artery bypass grafting.  

PubMed

Cardiopulmonary bypass is acknowledged to be one of the major causes of a complex systemic inflammatory response after cardiac surgery. Leukocyte-endothelial binding followed by neutrophil migration appears to play a central role. These interactions are mediated by adhesion molecules on the surface of activated cells. The present study compared the perioperative levels of soluble adhesion molecules after coronary artery bypass grafting (CABG) in patients with or without cardiopulmonary bypass (CPB). Altogether, 9 patients underwent off-pump revascularization and 11 did so with CPB. Plasma levels of soluble adhesion molecules sE-selectin and sP-selectin and soluble intercellular adhesion molecule-1 (sICAM-1) were measured before anesthesia induction and 1, 4, and 20 hours after reperfusion to the myocardium. The baseline plasma levels of the adhesion molecules were similar in the two groups. Perioperative levels of sE-selectin remained the same and did not differ between groups. Plasma sP-selectin increased in both groups, the change being significantly greater in the CPB group than that in the off-pump group (p = 0.001). Plasma sICAM-1 decreased during an early stage after CABG with CPB, recovering at 4 hours after reperfusion; and a significant increase in ICAM-1 was observed 20 hours later. In the off-pump group, sICAM-1 levels did not change at 1 and 4 hours after reperfusion but increased 20 hours later. Postoperative creatine kinase-muscle bound (CK-MB) levels were significantly higher in the CPB group than in the off-pump group (p = 0.001). The change in sP-selectin levels also showed a correlation with CK-MB values (r = 0.676, p = 0.001). The results indicated that off-pump revascularization is associated with reduced endothelial activation and myocardial injury. PMID:12616425

Wei, Minxin; Kuukasjärvi, Pekka; Laurikka, Jari; Kaukinen, Seppo; Iisalo, Pekka; Laine, Seppo; Tarkka, Matti

2003-02-01

115

Inside-out Signaling Promotes Dynamic Changes in the Carcinoembryonic Antigen-related Cellular Adhesion Molecule 1 (CEACAM1) Oligomeric State to Control Its Cell Adhesion Properties.  

PubMed

Cell-cell contacts are fundamental to multicellular organisms and are subject to exquisite levels of control. The carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) can engage in both cis-homophilic (parallel) oligomerization and trans-homophilic (anti-parallel) binding. In this study, we establish that the CEACAM1 transmembrane domain has a propensity to form cis-dimers via the transmembrane-embedded (432)GXXXG(436) motif and that this basal state is overcome when activated calmodulin binds to the CEACAM1 cytoplasmic domain. Although mutation of the (432)GXXXG(436) motif reduced CEACAM1 oligomerization, it did not affect surface localization of the receptor or influence CEACAM1-dependent cellular invasion by the pathogenic Neisseria. The mutation did, however, have a striking effect on CEACAM1-dependent cellular aggregation, increasing both the kinetics of cell-cell association and the size of cellular aggregates formed. CEACAM1 association with tyrosine kinase c-Src and tyrosine phosphatases SHP-1 and SHP-2 was not affected by the (432)GXXXG(436) mutation, consistent with their association with the monomeric form of wild type CEACAM1. Collectively, our results establish that a dynamic oligomer-to-monomer shift in surface-expressed CEACAM1 facilitates trans-homophilic binding and downstream effector signaling. PMID:24005674

Patel, Prerna C; Lee, Hannah S W; Ming, Aaron Y K; Rath, Arianna; Deber, Charles M; Yip, Christopher M; Rocheleau, Jonathan V; Gray-Owen, Scott D

2013-09-04

116

Vascular Cellular Adhesion Molecule-1 (VCAM-1) Expression in Mice Retinal Vessels Is Affected by Both Hyperglycemia and Hyperlipidemia  

PubMed Central

Background Inflammation has been proposed to be important in the pathogenesis of diabetic retinopathy. An early feature of inflammation is the release of cytokines leading to increased expression of endothelial activation markers such as vascular cellular adhesion molecule-1 (VCAM-1). Here we investigated the impact of diabetes and dyslipidemia on VCAM-1 expression in mouse retinal vessels, as well as the potential role of tumor necrosis factor-? (TNF?). Methodology/Principal Findings Expression of VCAM-1 was examined by confocal immunofluorescence microscopy in vessels of wild type (wt), hyperlipidemic (ApoE?/?) and TNF? deficient (TNF??/?, ApoE?/?/TNF??/?) mice. Eight weeks of streptozotocin-induced diabetes resulted in increased VCAM-1 in wt mice, predominantly in small vessels (<10 µm). Diabetic wt mice had higher total retinal TNF?, IL-6 and IL-1? mRNA than controls; as well as higher soluble VCAM-1 (sVCAM-1) in plasma. Lack of TNF? increased higher basal VCAM-1 protein and sVCAM-1, but failed to up-regulate IL-6 and IL-1? mRNA and VCAM-1 protein in response to diabetes. Basal VCAM-1 expression was higher in ApoE?/? than in wt mice and both VCAM-1 mRNA and protein levels were further increased by high fat diet. These changes correlated to plasma cholesterol, LDL- and HDL-cholesterol, but not to triglycerides levels. Diabetes, despite further increasing plasma cholesterol in ApoE?/? mice, had no effects on VCAM-1 protein expression or on sVCAM-1. However, it increased ICAM-1 mRNA expression in retinal vessels, which correlated to plasma triglycerides. Conclusions/Significance Hyperglycemia triggers an inflammatory response in the retina of normolipidemic mice and up-regulation of VCAM-1 in retinal vessels. Hypercholesterolemia effectively promotes VCAM-1 expression without evident stimulation of inflammation. Diabetes-induced endothelial activation in ApoE?/? mice seems driven by elevated plasma triglycerides but not by cholesterol. Results also suggest a complex role for TNF? in the regulation of VCAM-1 expression, being protective under basal conditions but pro-inflammatory in response to diabetes.

Gustavsson, Carin; Agardh, Carl-David; Zetterqvist, Anna V.; Nilsson, Jan; Agardh, Elisabet; Gomez, Maria F.

2010-01-01

117

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

118

Gamma-irradiation-induced Intercellular Adhesion Molecule1 (ICAM-1) Expression is Associated with Catalase: Activation of Ap1 and JNK  

Microsoft Academic Search

The ionizing radiation used in cancer therapy frequently produces damage to normal tissues and induces complex responses, including inflammation. The upregulation of the intercellular adhesion molecule-1 (ICAM-1) in response to numerous inducing factors is associated with inflammation. Therefore, this study examined the molecular mechanisms responsible for ICAM-1 expression induced by ?-irradiation (?IR). ICAM-1 mRNA and cell surface expression were induced

Eun-Wha Son; Dong-Kwon Rhee; Suhkneung Pyo

2006-01-01

119

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

120

Deletion of the carcinoembryonic antigen-related cell adhesion molecule 1 (Ceacam1) gene contributes to colon tumor progression in a murine model of carcinogenesis  

Microsoft Academic Search

Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) is a glycoprotein that is part of the carcinoembryonic antigen and the immunoglobulin superfamilies. We have shown that it functions as a tumor suppressor and that this function depends upon the presence of the longer CEACAM1 cytoplasmic domain. In this report, we describe the generation of a Ceacam1?\\/? mouse. The Ceacam1?\\/? colon exhibits

N Leung; C Turbide; M Olson; V Marcus; S Jothy; N Beauchemin

2006-01-01

121

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

122

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

123

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

PubMed

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 beta7-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 beta7-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 beta7-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 beta7-integrin. These results suggest the possibility that MAdCAM-1 may be largely involved in the lymphocyte recruitment in the gastritis mucosa with H. pylori. PMID:12390304

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

2002-11-01

124

The neutrophil-specific antigen CD177 is a counter-receptor for platelet endothelial cell adhesion molecule-1 (CD31).  

PubMed

Human neutrophil-specific CD177 (NB1 and PRV-1) has been reported to be up-regulated in a number of inflammatory settings, including bacterial infection and granulocyte-colony-stimulating factor application. Little is known about its function. By flow cytometry and immunoprecipitation studies, we identified platelet endothelial cell adhesion molecule-1 (PECAM-1) as a binding partner of CD177. Real-time protein-protein analysis using surface plasmon resonance confirmed a cation-dependent, specific interaction between CD177 and the heterophilic domains of PECAM-1. Monoclonal antibodies against CD177 and against PECAM-1 domain 6 inhibited adhesion of U937 cells stably expressing CD177 to immobilized PECAM-1. Transendothelial migration of human neutrophils was also inhibited by these antibodies. Our findings provide direct evidence that neutrophil-specific CD177 is a heterophilic binding partner of PECAM-1. This interaction may constitute a new pathway that participates in neutrophil transmigration. PMID:17580308

Sachs, Ulrich J H; Andrei-Selmer, Cornelia L; Maniar, Amudhan; Weiss, Timo; Paddock, Cathy; Orlova, Valeria V; Choi, Eun Young; Newman, Peter J; Preissner, Klaus T; Chavakis, Triantafyllos; Santoso, Sentot

2007-06-19

125

Rational Design of Anticytoadherence Inhibitors for Plasmodium falciparum Based on the Crystal Structure of Human Intercellular Adhesion Molecule 1  

Microsoft Academic Search

Received 23 September 2005\\/Returned for modification 22 October 2005\\/Accepted 12 November 2005 Adhesion of Plasmodium falciparum-infected erythrocytes (IE) to host endothelium has been associated with pathology in malaria. Although the interaction with endothelial cells can be complex due to the relatively large number of host receptors available for binding, specific proteins have been identified that are more commonly used than

Matthias Dormeyer; Yvonne Adams; Bernd Kramer; Srabasti Chakravorty; Man Tsuey Tse; Stefano Pegoraro; Lisa Whittaker; Michael Lanzer; Alister Craig

2006-01-01

126

Suppression of complement regulatory protein C1 inhibitor in vascular endothelial activation by inhibiting vascular cell adhesion molecule-1 action  

SciTech Connect

Increased expression of adhesion molecules by activated endothelium is a critical feature of vascular inflammation associated with the several diseases such as endotoxin shock and sepsis/septic shock. Our data demonstrated complement regulatory protein C1 inhibitor (C1INH) prevents endothelial cell injury. We hypothesized that C1INH has the ability of an anti-endothelial activation associated with suppression of expression of adhesion molecule(s). C1INH blocked leukocyte adhesion to endothelial cell monolayer in both static assay and flow conditions. In inflammatory condition, C1INH reduced vascular cell adhesion molecule (VCAM-1) expression associated with its cytoplasmic mRNA destabilization and nuclear transcription level. Studies exploring the underlying mechanism of C1INH-mediated suppression in VCAM-1 expression were related to reduction of NF-{kappa}B activation and nuclear translocation in an I{kappa}B{alpha}-dependent manner. The inhibitory effects were associated with reduction of inhibitor I{kappa}B kinase activity and stabilization of the NF-{kappa}B inhibitor I{kappa}B. These findings indicate a novel role for C1INH in inhibition of vascular endothelial activation. These observations could provide the basis for new therapeutic application of C1INH to target inflammatory processes in different pathologic situations.

Zhang, Haimou [Center for Infection and Immunity Research, School of Life Sciences, Hubei University, Wuhan, Hubei (China); Qin, Gangjian [Feinberg Cardiovascular Research Institute, Northwestern University Feinberg School of Medicine, Chicago, IL (United States); Liang, Gang [Children's Hospital, Harvard Medical School, Boston, MA (United States); Li, Jinan [CBR Institute for Biomedical Research, Harvard Medical School, Boston, MA (United States); Chiu, Isaac [CBR Institute for Biomedical Research, Harvard Medical School, Boston, MA (United States); Barrington, Robert A. [CBR Institute for Biomedical Research, Harvard Medical School, Boston, MA (United States); Liu, Dongxu [Center for Infection and Immunity Research, School of Life Sciences, Hubei University, Wuhan, Hubei (China)]. E-mail: dxliu001@yahoo.com

2007-07-13

127

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

128

The Fasciclin-Like Arabinogalactan Proteins of Arabidopsis. A Multigene Family of Putative Cell Adhesion Molecules1  

PubMed Central

Fasciclin-like arabinogalactan proteins (FLAs) are a subclass of arabinogalactan proteins (AGPs) that have, in addition to predicted AGP-like glycosylated regions, putative cell adhesion domains known as fasciclin domains. In other eukaryotes (e.g. fruitfly [Drosophila melanogaster] and humans [Homo sapiens]), fasciclin domain-containing proteins are involved in cell adhesion. There are at least 21 FLAs in the annotated Arabidopsis genome. Despite the deduced proteins having low overall similarity, sequence analysis of the fasciclin domains in Arabidopsis FLAs identified two highly conserved regions that define this motif, suggesting that the cell adhesion function is conserved. We show that FLAs precipitate with ?-glucosyl Yariv reagent, indicating that they share structural characteristics with AGPs. Fourteen of the FLA family members are predicted to be C-terminally substituted with a glycosylphosphatidylinositol anchor, a cleavable form of membrane anchor for proteins, indicating different FLAs may have different developmental roles. Publicly available microarray and expressed sequence tag data were used to select FLAs for further expression analysis. RNA gel blots for a number of FLAs indicate that they are likely to be important during plant development and in response to abiotic stress. FLAs 1,2, and 8 show a rapid decrease in mRNA abundance in response to the phytohormone abscisic acid. Also, the accumulation of FLA1 and FLA2 transcripts differs during callus and shoot development, indicating that the proteins may be significant in the process of competence acquisition and induction of shoot development.

Johnson, Kim L.; Jones, Brian J.; Bacic, Antony; Schultz, Carolyn J.

2003-01-01

129

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

130

A preparation of herbal medicine Salvia miltiorrhiza reduces expression of intercellular adhesion molecule-1 and development of atherosclerosis in apolipoprotein E-deficient mice.  

PubMed

Cardiotonic pill (CP) is a pharmaceutical preparation of the herbal medicine Salvia miltiorrhiza. In vitro studies demonstrate that CP inhibits vascular endothelial expression of adhesion molecules and smooth-muscle proliferation, implying the possibility of antiatherosclerotic effects. This study employs an in vivo animal model to examine the potential therapeutic efficacy of CP on atherosclerotic development. Male apolipoprotein E-deficient (ApoE-/-) mice fed with an atherogenic (high fat) diet were administered with CP (90-120 mg/kg per day) via drinking water for 8 weeks. Hypercholesterolemia developed in the mice, with 22-fold increases in plasma levels of total cholesterol, 29-fold of LDL, and 7-fold of HDL. CP therapy did not significantly alter the lipid levels. Expression of intercellular adhesion molecule 1 significantly increased in circulating leukocytes and was abolished by CP therapy. Atherosclerosis significantly developed in the aorta and was attenuated by CP therapy, with an approximately 30% reduction in whole atherosclerotic lesions and an approximately 50% reduction in fibrous plaques in the artery. Thus, herbal medicine CP partly protects ApoE-/- mice from high-fat diet-induced atherogenesis. The protection is unlikely to be attributable to decreases in circulating cholesterol levels, but it might possibly relate to an inhibition of expression of adhesion molecules and other effects that remain unknown at this time. PMID:18209567

Ling, Shanhong; Dai, Aozhi; Guo, Zhixin; Komesaroff, Paul A

2008-01-01

131

Adhesion molecule expression in Graves' thyroid glands; potential relevance of granule membrane protein (GMP-140) and intercellular adhesion molecule-1 (ICAM-1) in the homing and antigen presentation processes.  

PubMed Central

To assess the potential role of adhesion molecules in the pathogenesis of Graves' disease, we examined the expression of several of these adhesion molecules, including intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule (VCAM-1) and granule membrane protein-140 (GMP-140), in sections of Graves' thyroid glands and control thyroids, using immunohistochemical techniques. Up-regulated expression of GMP-140 was frequently observed on endothelial cells (EC) of post-capilliary venules in all Graves' thyroids examined, compared with an occasional weak staining on EC control glands. Some capillary EC around thyroid follicles (perifollicular EC) were strongly positive for GMP-140 in the Graves' thyroids in contrast to a negative staining on the same structures in the control glands. In addition, there was a correlation between the reactivity and frequency of GMP-140 expression on EC and the severity of mononuclear cell (MNC) infiltration in the Graves' thyroids. The expression of ICAM-1 was up-regulated on perifollicular EC and EC of small venules in some thyroids of both Graves' and control groups. Conversely, no significant expression was observed on any type of EC for both endothelial-leucocyte adhesion molecule-1 (ELAM-1) and VCAM-1. However, dendritic-like cells, present within lymphocytic infiltrates, were positive for VCAM-1 in most of the Graves' thyroids examined, especially in those with a severe lymphocytic infiltration. Thyrocytes were constantly negative for the expression of all four adhesion molecules investigated. These data suggest that GMP-140, as well as ICAM-1, could play an important role in the initiation of MNC infiltration in Graves' disease. ELAM-1 and VCAM-1 appear not to be relevant for the migration of MNC from the blood vessels into the target gland, although VCAM-1 expression on dendritic-like cells might play an additively tissue-selective role in autoantigen presentation and subsequent elicitation of autoimmune phenomena.

Miyazaki, A; Mirakian, R; Bottazzo, G F

1992-01-01

132

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 Central

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.

Meyer, Michael Andrew

2013-01-01

133

Possible mechanism of the anti-inflammatory activity of ruscogenin: role of intercellular adhesion molecule-1 and nuclear factor-kappaB.  

PubMed

Ruscogenin (RUS), first isolated from Ruscus aculeatus, also a major steroidal sapogenin of traditional Chinese herb Radix Ophiopogon japonicus, has been found to exert significant anti-inflammatory and anti-thrombotic activities. Our previous studies suggested that ruscogenin remarkably inhibited adhesion of leukocytes to a human umbilical vein endothelial cell line (ECV304) injured by tumor necrosis factor-alpha (TNF-alpha) in a concentration-dependent manner. Yet the underlying mechanisms remain unclear. In this study, the in vivo effects of ruscogenin on leukocyte migration and celiac prostaglandin E(2) (PGE(2)) level induced by zymosan A were studied in mice. Furthermore, the effects of ruscogenin on TNF-alpha-induced intercellular adhesion molecule-1 (ICAM-1) expression and nuclear factor-kappaB (NF-kappaB) activation were also investigated under consideration of their key roles in leukocyte recruitment. The results showed that ruscogenin significantly suppressed zymosan A-evoked peritoneal total leukocyte migration in mice in a dose-dependent manner, while it had no obvious effect on PGE(2) content in peritoneal exudant. Ruscogenin also inhibited TNF-alpha-induced over expression of ICAM-1 both at the mRNA and protein levels and suppressed NF-kappaB activation considerably by decreasing NF-kappaB p65 translocation and DNA binding activity. These findings provide some new insights that may explain the possible molecular mechanism of ruscogenin and Radix Ophiopogon japonicus for the inhibition of endothelial responses to cytokines during inflammatory and vascular disorders. PMID:18946195

Huang, Ya-Lin; Kou, Jun-Ping; Ma, Li; Song, Jia-Xi; Yu, Bo-Yang

2008-10-01

134

Artemether Combined with shRNA Interference of Vascular Cell Adhesion Molecule-1 Significantly Inhibited the Malignant Biological Behavior of Human Glioma Cells  

PubMed Central

Artemether is the derivative extracted from Chinese traditional herb and originally used for malaria. Artemether also has potential therapeutic effects against tumors. Vascular cell adhesion molecule-1 (VCAM-1) is an important cell surface adhesion molecule associated with malignancy of gliomas. In this work, we investigated the role and mechanism of artemether combined with shRNA interference of VCAM-1 (shRNA-VCAM-1) on the migration, invasion and apoptosis of glioma cells. U87 human glioma cells were treated with artemether at various concentrations and shRNA interfering technology was employed to silence the expression of VCAM-1. Cell viability, migration, invasiveness and apoptosis were assessed with MTT, wound healing, Transwell and Annexin V-FITC/PI staining. The expression of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9) and phosphorylated Akt (p-Akt) was checked by Western blot assay. Results showed that artemether and shRNA-VCAM-1 not only significantly inhibited the migration, invasiveness and expression of MMP-2/9 and p-Akt, but also promoted the apoptosis of U87 cells. Combined treatment of both displayed the maximum inhibitory effects on the malignant biological behavior of glioma cells. Our work revealed the potential therapeutic effects of artemether and antiVCAM-1 in the treatments of gliomas.

Wang, Ping; Xue, Yi-Xue; Yao, Yi-Long; Yu, Bo; Liu, Yun-Hui

2013-01-01

135

Cell adhesion molecule 1 (CADM1) is ubiquitously present in the endothelium and smooth muscle cells of the human macro- and micro-vasculature.  

PubMed

Cell adhesion molecule 1 (CADM1) is a member of the immunoglobulin cell adhesion molecule family. Recently, we identified CADM1 to be a novel risk factor for venous thrombosis in a large, protein C deficient, thrombophilic family and showed, for the first time, the expression of CADM1 in endothelial cells (Hasstedt et al. in Blood 114:3084-3091, 2009). To further investigate its role in venous thrombosis, as well as other vasculopathies, we undertook a systematic confocal microscopic investigation for the presence of CADM1 in the vasculature of 28 different human tissues. Paraffin embedded tissue sections were dual immunostained with an antibody against CADM1, together with an antibody against either von Willebrand factor (to identify endothelial cells), or ?-smooth muscle actin (to identify smooth muscle cells). The results showed that CADM1 was ubiquitously present in endothelial cells and smooth muscle cells in the vasculature from all 28 tissues, though its representation in the various classes of vessels was tissue dependent. PMID:22940845

Tatsumi, Kanayo; Taatjes, Douglas J; Wadsworth, Marilyn P; Bouchard, Beth A; Bovill, Edwin G

2012-09-01

136

Expression of major histocompatibility class I and class II antigens and intercellular adhesion molecule-1 on operable non-small cell lung carcinomas: frequency and prognostic significance.  

PubMed

Major histocompatibility complex (MHC) antigens and adhesion molecules, such as the intercellular adhesion molecule-1 (ICAM-1), appear to play an important role in the immunological recognition and destruction of tumour cells. We, therefore, examined the expression patterns of these proteins on primary tumours of 91 patients with operable non-small cell lung cancer (NSCLC). Applying immunohistochemistry with monoclonal antibody (MAb) W6/32 against a common framework determinant of HLA class I antigens revealed a deficient expression in 33.0% of the cases analysed, while neo-expression of either HLA class II antigens (MAb TAL.1B5) or ICAM-1 (MAb PA3.58-14) was observed in 26.4 or 29.7% of tumours, respectively. Analysis of consecutive tumour specimens indicated that HLA antigens and ICAM-1 were frequently coexpressed. With regard to clinicopathological risk factors, we could demonstrate a preferential expression of those markers in patients with locally restricted and well-differentiated tumours or no lymph node metastases, which was more pronounced in adenocarcinomas than in squamous cell carcinomas. In contrast, the presence versus the absence of HLA antigens and ICAM-1 was not correlated with the rate of tumour recurrence or overall survival in patients with NSCLC. In conclusion, the co-ordinated expression of immunologically relevant cell surface molecules on primary NSCLC is a frequent event that correlates with distinct parameters of favourable prognosis. However, we have no evidence that the immune response facilitated by these molecules can effectively influence the clinical course of the disease. PMID:8204362

Passlick, B; Izbicki, J R; Simmel, S; Kubuschok, B; Karg, O; Habekost, M; Thetter, O; Schweiberer, L; Pantel, K

1994-01-01

137

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

138

Activation of Intercellular Adhesion Molecule 1 Expression by Helicobacter pylori Is Regulated by NF-?B in Gastric Epithelial Cancer Cells  

PubMed Central

Interactions between leukocytes and epithelial cells may play a key role in Helicobacter pylori-associated gastric mucosal inflammation. This process is mediated by various cell adhesion molecules. The present study examined the molecular mechanisms leading to H. pylori-induced epithelial cell intercellular adhesion molecule-1 (ICAM-1; also called CD54) expression. Coculture of epithelial cells with cytotoxin-associated gene pathogenicity island-positive (cag PAI+) H. pylori strains, but not with a cag PAI? strain or H. pylori culture supernatants, resulted in upregulation of steady-state mRNA levels and cell surface expression of ICAM-1. Coculture with H. pylori induced an increase in luciferase activity in cells which were transfected with a luciferase reporter gene linked to the 5?-flanking region of the ICAM-1 gene. H. pylori activated the ICAM-1 promoter via the NF-?B binding site. An inducible nuclear protein complex bound to the ICAM-1 NF-?B site and was identified as the NF-?B p50–p65 heterodimer. H. pylori induced the degradation of I?B-?, a major cytoplasmic inhibitor of NF-?B, and stimulated the expression of I?B-? mRNA. Pretreatment of epithelial cells with pyrrolidine dithiocarbamate, which blocks NF-?B activation, inhibited H. pylori-induced ICAM-1 expression. THP-1 macrophagic cells, peripheral blood mononuclear cells, and purified neutrophils adhered to H. pylori-infected epithelial cells to a greater extent than to uninfected cells. These results show that H. pylori directly induces expression of ICAM-1 on gastric epithelial cells in an NF-?B-dependent manner that may support leukocyte attachment during inflammation.

Mori, Naoki; Wada, Akihiro; Hirayama, Toshiya; Parks, Thomas P.; Stratowa, Christian; Yamamoto, Naoki

2000-01-01

139

Peptides derived from the complementarity-determining regions of anti-Mac-1 antibodies block intercellular adhesion molecule-1 interaction with Mac-1.  

PubMed

Peptides or small molecules that can block the interaction of the integrin Mac-1 with its receptor, intercellular adhesion molecule-1 (ICAM-1), have not previously been developed. We studied this interaction by measuring the adherence of ICAM-1-expressing Chinese hamster ovary (CHO) cells to immobilized, purified Mac-1. Nucleotide sequence information was obtained for the complementarity determining regions (CDRs) of three antibodies (44aacb, MY904, and 118.1) shown to block Mac-1-mediated cell adherence. Peptides were synthesized based on the predicted amino acid sequences of the CDRs and tested for the ability to block cell adhesion to Mac-1. Peptides derived from CDR1 of 44aacb, CDR2 of 118.1, and CDRs 1 and 3 of MY904 heavy chains were found to possess blocking activity at 10-100 muM. This may indicate that one or two CDRs contribute disproportionately to the antibody binding affinity. The binding of ligands to Mac-1 has been shown to require a region of the alpha-chain known as the I- or A-domain. We have recombinantly produced Mac-1 I-domain, and show that it is also capable of supporting the adherence of ICAM-1-expressing CHO cells. The adherence of ICAM-1-CHO cells to the I-domain is inhibited by 44aacb and 118.1 and by the CDR peptides from 44aacb and 118.1. By using phage display of peptide libraries based on the 118.1 CDR peptide with five residues randomized, we were able to identify a novel peptide inhibitor of Mac-1 with substitutions at all five positions. These peptides provide lead structures for development of Mac-1 antagonists. PMID:9488691

Feng, Y; Chung, D; Garrard, L; McEnroe, G; Lim, D; Scardina, J; McFadden, K; Guzzetta, A; Lam, A; Abraham, J; Liu, D; Endemann, G

1998-03-01

140

Asymmetric Dimethylarginine (ADMA) and Soluble Vascular Cell Adhesion Molecule 1(sVCAM-1) as Circulating Markers for Endothelial Dysfunction in Patients with Pheochromocytoma.  

PubMed

Endothelial dysfunction is a common feature of hypertension and is associated with reduced nitric oxide bioavailability. The endogenous inhibitor of nitric oxide syntase, asymmetric dimethylarginine (ADMA), and soluble adhesion molecules such as vascular cell adhesion molecule 1 (sVCAM-1) have been established as markers of endothelial dysfunction in a number of pathologic conditions including essential hypertension. There is little information, however, about these markers in endocrine hypertension.To investigate the levels of circulating ADMA and sVCAM-1 in patients with pheochromocytoma.Serum ADMA and sVCAM-1 concentrations were assayed by ELISA technique in 18 patients with pheochromocytoma, 18 patients with essential hypertension (EH) and 18 healthy subjects serving as a control group.ADMA and sVCAM-1 levels were significantly elevated in pheochromocytoma patients compared to normotensive healthy controls (0.479±0.072 vs. 0.433±0.054 µmol/l, p=0.037 and 690±181 vs. 577±108 ng/ml, p=0.03, respectively). Patients with EH also had higher ADMA concentrations than the control group, but the difference was not significant (0.476±0.075 vs. 0.433±0.054 µmol/l, p=0.06). No associations were found between the levels of ADMA, sVCAM-1 and some potential risk factors for endothelial dysfunction.Endothelial function is impaired in patients with pheochromocytoma as indicated by the elevated circulating levels of ADMA and sVCAM-1. The lack of association of these markers with cateholamines, glucose and lipid abnormalities together with their comparable levels in EH patients suggests that endothelial dysfunction is most likely related to hypertension itself. PMID:24002898

Vasilev, V; Matrozova, J; Elenkova, A; Vandeva, S; Kirilov, G; Zacharieva, S

2013-09-03

141

Prostaglandin E2/EP1 Signaling Pathway Enhances Intercellular Adhesion Molecule 1 (ICAM-1) Expression and Cell Motility in Oral Cancer Cells*  

PubMed Central

Oral squamous cell carcinoma has a striking tendency to migrate and metastasize. Cyclooxygenase (COX)-2, the inducible isoform of prostaglandin (PG) synthase, has been implicated in tumor metastasis. However, the effects of COX-2 on human oral cancer cells are largely unknown. We found that overexpression of COX-2 or exogenous PGE2 increased migration and intercellular adhesion molecule 1 (ICAM)-1 expression in human oral cancer cells. Using pharmacological inhibitors, activators, and genetic inhibition of EP receptors, we discovered that the EP1 receptor, but not other PGE receptors, is involved in PGE2-mediated cell migration and ICAM-1 expression. PGE2-mediated migration and ICAM-1 up-regulation were attenuated by inhibitors of protein kinase C (PKC)?, and c-Src. Activation of the PKC?, c-Src, and AP-1 signaling pathway occurred after PGE2 treatment. PGE2-induced expression of ICAM-1 and migration activity were inhibited by a specific inhibitor, siRNA, and mutants of PKC?, c-Src, and AP-1. In addition, migration-prone sublines demonstrated that cells with increased migration ability had higher expression of COX-2 and ICAM-1. Taken together, these results indicate that the PGE2 and EP1 interaction enhanced migration of oral cancer cells through an increase in ICAM-1 production.

Yang, Shun-Fa; Chen, Mu-Kuan; Hsieh, Yih-Shou; Chung, Tsung-Te; Hsieh, Yi-Hsien; Lin, Chiao-Wen; Su, Jen-Liang; Tsai, Ming-Hsui; Tang, Chih-Hsin

2010-01-01

142

Reducing agents inhibit rhinovirus-induced up-regulation of the rhinovirus receptor intercellular adhesion molecule-1 (ICAM-1) in respiratory epithelial cells.  

PubMed

Rhinoviruses are the major cause of common colds and of asthma exacerbations. Intercellular adhesion molecule-1 (ICAM-1) has a central role in airway inflammation and is the receptor for 90% of rhinoviruses. Rhinovirus infection of airway epithelium induces ICAM-1. Because redox state is directly implicated in inflammatory responses via molecular signaling mechanisms, here we studied the effects of reducing agents on rhinovirus-induced ICAM-1 expression, mRNA up-regulation, promoter activation, and nuclear factor activation. To investigate the effects of rhinovirus infection on the intracellular redox balance, we also studied whether rhinovirus infection triggers the production of reactive oxygen species. We found that reduced (GSH) but not oxidized (GSSG) glutathione (1-100 microM) inhibited in a dose-dependent manner rhinovirus-induced ICAM-1 up-regulation and mRNA induction in primary bronchial and A549 respiratory epithelial cells. GSH but not GSSG also inhibited rhinovirus-induced ICAM-1 promoter activation and rhinovirus-induced NF-kB activation. In parallel, we found that rhinovirus infection induced a rapid increase of intracellular superoxide anion that was maximal at the time of NF-kB activation. This oxidant generation was completely inhibited by GSH. We conclude that redox-mediated intracellular pathways represent an important target for the therapeutic control of rhinovirus-induced diseases. PMID:12368227

Papi, Alberto; Papadopoulos, Nikolaos G; Stanciu, Luminita A; Bellettato, Cinzia M; Pinamonti, Silvano; Degitz, Klaus; Holgate, Stephen T; Johnston, Sebastian L

2002-10-04

143

Glycosylation-dependent cell adhesion molecule 1 (GlyCAM 1) mucin is expressed by lactating mammary gland epithelial cells and is present in milk.  

PubMed Central

Glycosylation-dependent cell adhesion molecule 1 (GlyCAM 1) is a mucinlike endothelial glycoprotein that acts as an adhesive ligand for L selectin by presenting one or more O-linked carbohydrates to the lectin domain of this leukocyte cell surface selectin. The GlyCAM 1 glycoprotein has been previously shown to be expressed specifically by the endothelial cells of peripheral and mesenteric lymph nodes and in an unknown site in lung. Here we report that this protein is also expressed during lactation by mammary epithelial cells. Northern blot analysis has shown that the mRNA for GlyCAM 1 appears to be induced during pregnancy in a manner similar to that previously described for hormonally induced milk proteins. In situ hybridization analysis reveals that the site of GlyCAM 1 synthesis in the mammary gland is in the epithelial cells that produce these same milk proteins. Immunohistochemistry of mammary glands using antisera directed against GlyCAM 1 peptides demonstrates that these epithelial cells contain GlyCAM 1 protein, and that this protein is also found lumenally in the milk of the secreting mammary gland. Analysis of murine milk shows that immunoreactive GlyCAM 1 is found in the soluble whey fraction. Finally, labeling analysis of milk GlyCAM 1 has demonstrated that this form of the glycoprotein lacks the sulfate-modified carbohydrate that has recently been shown to be required for the ligand binding activity to L selectin. The nonsulfated mammary GlyCAM 1 is unable to interact with L selectin, consistent with the hypothesis that milk GlyCAM 1 has a different function than endothelial GlyCAM 1. These data thus suggest that milk GlyCAM 1 is a hormonally regulated milk protein that is part of the milk mucin complex. In addition, the finding that the mammary form of GlyCAM 1 contains different carbohydrate modifications than the endothelial form suggests that this glycoprotein may be a scaffold for carbohydrates that mediate functions in addition to cell adhesion. Images

Dowbenko, D; Kikuta, A; Fennie, C; Gillett, N; Lasky, L A

1993-01-01

144

Interleukin-8 and intercellular adhesion molecule 1 regulation in oral epithelial cells by selected periodontal bacteria: multiple effects of Porphyromonas gingivalis via antagonistic mechanisms.  

PubMed

Interaction of bacteria with mucosal surfaces can modulate the production of proinflammatory cytokines and adhesion molecules produced by epithelial cells. Previously, we showed that expression of interleukin-8 (IL-8) and intercellular adhesion molecule 1 (ICAM-1) by gingival epithelial cells increases following interaction with several putative periodontal pathogens. In contrast, expression of IL-8 and ICAM-1 is reduced after Porphyromonas gingivalis ATCC 33277 challenge. In the present study, we investigated the mechanisms that govern the regulation of these two molecules in bacterially infected gingival epithelial cells. Experimental approaches included bacterial stimulation of gingival epithelial cells by either a brief challenge (1.5 to 2 h) or a continuous coculture throughout the incubation period. The kinetics of IL-8 and ICAM-1 expression following brief challenge were such that (i) secretion of IL-8 by gingival epithelial cells reached its peak 2 h following Fusobacterium nucleatum infection whereas it rapidly decreased within 2 h after P. gingivalis infection and remained decreased up to 30 h and (ii) IL-8 and ICAM-1 mRNA levels were up-regulated rapidly 2 to 4 h postinfection and then decreased to basal levels 8 to 20 h after infection with either Actinobacillus actinomycetemcomitans, F. nucleatum, or P. gingivalis. Attenuation of IL-8 secretion was facilitated by adherent P. gingivalis strains. The IL-8 secreted from epithelial cells after F. nucleatum stimulation could be down-regulated by subsequent infection with P. gingivalis or its culture supernatant. Although these results suggested that IL-8 attenuation at the protein level might be associated with P. gingivalis proteases, the Arg- and Lys-gingipain proteases did not appear to be solely responsible for IL-8 attenuation. In addition, while P. gingivalis up-regulated IL-8 mRNA expression, this effect was overridden when the bacteria were continuously cocultured with the epithelial cells. The IL-8 mRNA levels in epithelial cells following sequential challenge with P. gingivalis and F. nucleatum and vice versa were approximately identical and were lower than those following F. nucleatum challenge alone and higher than control levels or those following P. gingivalis challenge alone. Thus, together with the protease effect, P. gingivalis possesses a powerful strategy to ensure the down-regulation of IL-8 and ICAM-1. PMID:11179300

Huang, G T; Kim, D; Lee, J K; Kuramitsu, H K; Haake, S K

2001-03-01

145

Expression of various MHC class II molecules and of intracellular adhesion molecule-1 (ICAM-1) on focal clusters of dendritic cells in iodine deficiency goitres  

PubMed Central

Thyroid sections from 18 consecutive euthyroid patients undergoing surgery for iodine deficiency goitre were investigated by means of immunohistochemistry and immunofluorescence, evaluating the expression of MHC class II antigens (HLA-DR, -DP, -DQ, and RFD1) and intercellular adhesion molecule-1 on the formerly described clusters of dendritic cells, as well as on thyrocytes. Eleven of 18 iodine deficiency goitres contained clusters of dendritic cells. These clusters appeared to express only HLA-DR in two cases; in nine of 12 cases they showed a differential expression of class II molecules in the following frequency: HLA-DR>DQ and/or -DP>RFD1. These dendritic cells also were ICAM-1+. In four of 18 iodine deficiency goitres, thyroid epithelial cells showed MHC class II expression in several combinations, but were ICAM-1-. In normal thyroids and in nodular goitres from inhabitants of the endemic area not having an actual iodine deficiency, only sparse clusters of dendritic cells were found; these cells were only HLA-DR+. Follicle lining cells were negative for the MHC class II molecules. In normal thyroids from an area with sufficient iodine supply, no clusters of dendritic cells were seen. The few dendritic cells observed were lying isolated in the interstitium and only positive for HLA-DR and ICAM-1; epithelial cells were negative for the studied markers. These data show clusters of dendritic cells in thyroids of inhabitants of an endemic area. When goitre is accompanied by iodine deficiency at the moment of operation, there appears to be activation of these dendritic cells and of thyroid epithelial cells. ImagesFig. 1Fig. 2

Dimal, P.; Wilders-Truschnig, M.; Mooij, P.; Leb, G.; Eber, O.; Langsteger, W.; Hebenstreit, J.; Beham, A.; Stiegler, C.; Dohr, G.; Drexhage, H. A.

1993-01-01

146

Rhinovirus infection induces expression of its own receptor intercellular adhesion molecule 1 (ICAM-1) via increased NF-kappaB-mediated transcription.  

PubMed

Virus infections, the majority of which are rhinovirus infections, are the major cause of asthma exacerbations. Treatment is unsatisfactory, and the pathogenesis unclear. Lower airway lymphocyte and eosinophil recruitment and activation are strongly implicated, but the mechanisms regulating these processes are unknown. Intercellular adhesion molecule-1 (ICAM-1) has a central role in inflammatory cell recruitment to the airways in asthma and is the cellular receptor for 90% of rhinoviruses. We hypothesized that rhinovirus infection of lower airway epithelium might induce ICAM-1 expression, promoting both inflammatory cell infiltration and rhinovirus infection. We therefore investigated the effect of rhinovirus infection on respiratory epithelial cell ICAM-1 expression and regulation to identify new targets for treatment of virus-induced asthma exacerbations. We observed that rhinovirus infection of primary bronchial epithelial cells and the A549 respiratory epithelial cell line increased ICAM-1 cell surface expression over 12- and 3-fold, respectively. We then investigated the mechanisms of this induction in A549 cells and observed rhinovirus-induction of ICAM-1 promoter activity and ICAM-1 mRNA transcription. Rhinovirus induction of ICAM-1 promoter activity was critically dependent upon up-regulation of NF-kappaB proteins binding to the -187/-178 NF-kappaB binding site on the ICAM-1 promoter. The principal components of the rhinovirus-induced binding proteins were NF-kappaB p65 homo- or heterodimers. These studies identify ICAM-1 and NF-kappaB as new targets for the development of therapeutic interventions for virus-induced asthma exacerbations. PMID:10092659

Papi, A; Johnston, S L

1999-04-01

147

Role of JNK and NF??B pathways in Porphyromonas gingivalis LPS?induced vascular cell adhesion molecule?1 expression in human aortic endothelial cells.  

PubMed

An increasing number of studies have shown a correlation between Porphyromonas gingivalis (P. gingivalis) infection and atherosclerosis. A recent study demonstrated that the expression of vascular cell adhesion molecule?1 (VCAM?1) was induced by P. gingivalis lipopolysaccharide (LPS) in human aortic endothelial cells (HAECs). The activation of p38 mitogen?activated protein kinase (p38 MAPK) was at least partially involved in this process. Those results suggested the potential involvement of P. gingivalis LPS in the pathogenesis of atherosclerosis. However, the mechanism involved in P. gingivalis LPS?induced VCAM?1 production has not yet been elucidated. The present study examined the role of the c?Jun N?terminal kinase (JNK) and nuclear factor??B (NF??B) cell signaling pathways in P. gingivalis LPS?induced VCAM?1 expression in HAECs. Western blotting was used to investigate the activation of JNK and NF??B pathways in HAECs exposed to P. gingivalis LPS. Following this, specific pharmacological inhibitors were introduced and the protein production of VCAM?1 was studied. The results showed that the JNK and NF??B pathways in HAECs were capable of being activated by P. gingivalis LPS. The inhibition of NF??B by SN50 significantly attenuated P. gingivalis LPS?induced VCAM?1 expression, while the inhibition of JNK by SP600125 enhanced VCAM?1 expression in P. gingivalis LPS?treated HAECs. Therefore, the results indicated that NF??B was essential for the P. gingivalis LPS?induced VCAM?1 expression in HAECs and that JNK may be a suppressor of VCAM?1 expression in HAECs. PMID:24045414

Liu, Bin; Wang, Jia; Cheng, Lan; Liang, Jingping

2013-09-17

148

Inhibition of endothelial vascular cell adhesion molecule-1 expression by nitric oxide involves the induction and nuclear translocation of IkappaBalpha.  

PubMed

The induction of vascular cell adhesion molecule-1 (VCAM-1) expression by tumor necrosis factor (TNF)-alpha requires the activation of nuclear factor-kappaB (NF-kappaB) via a process involving the phosphorylation and degradation of its cytoplasmic inhibitor, IkappaBalpha. We have shown that nitric oxide (NO) decreases VCAM-1 expression via inhibition of NF-kappaB activation. To determine how NO inhibits NF-kappaB, we studied the fate of IkappaBalpha following TNF-alpha stimulation in the presence of NO donors S-nitrosoglutathione and sodium nitroprusside. Activation of NF-kappaB by TNF-alpha occurred within 15 min and coincided with rapid degradation of IkappaBalpha. Co-treatment with NO donors did not prevent IkappaBalpha phosphorylation or degradation. However, after 2 h of TNF-alpha stimulation, NO donors inhibited NF-kappaB activation and augmented IkappaBalpha resynthesis and nuclear translocation by 2.5- and 3-fold, respectively. This correlated with a 75% reduction in TNF-alpha-induced VCAM-1 expression. In a time-dependent manner, NO donors alone caused the nuclear translocation of IkappaBalpha. To confirm that NO donors have similar effects as endogenously derived NO, murine macrophage-like cells, RAW264.7, were co-cultured with endothelial cells. Induction of RAW264.7-derived NO inhibited lipopolysaccharide-induced endothelial VCAM-1 expression, which was reversed by the NO synthase inhibitor Nomega-monomethyl-L-arginine. These findings indicate that NO inhibits NF-kappaB activation and VCAM-1 expression by increasing the expression and nuclear translocation of IkappaBalpha. PMID:9388244

Spiecker, M; Peng, H B; Liao, J K

1997-12-01

149

Leukocyte function-associated antigen-1/intercellular adhesion molecule-1 interaction induces a novel genetic signature resulting in T-cells refractory to transforming growth factor-? signaling.  

PubMed

The immunesuppressive cytokine TGF-? plays crucial regulatory roles in the induction and maintenance of immunologic tolerance and prevention of immunopathologies. However, it remains unclear how circulating T-cells can escape from the quiescent state maintained by TGF-?. Here, we report that the T-cell integrin leukocyte function-associated antigen-1 (LFA-1) interaction with its ligand intercellular adhesion molecule-1 (ICAM-1) induces a genetic signature associated with reduced TGF-? responsiveness via up-regulation of SKI, E3 ubiquitin-protein ligase SMURF2, and SMAD7 (mothers against decapentaplegic homolog 7) genes and proteins. We confirmed that the expression of these TGF-? inhibitory molecules was dependent on STAT3 and/or JNK activation. Increased expression of SMAD7 and SMURF2 in LFA-1/ICAM-1 cross-linked T-cells resulted in impaired TGF-?-mediated phosphorylation of SMAD2 and suppression of IL-2 secretion. Expression of SKI caused resistance to TGF-?-mediated suppression of IL-2, but SMAD2 phosphorylation was unaffected. Blocking LFA-1 by neutralizing antibody or specific knockdown of TGF-? inhibitory molecules by siRNA substantially restored LFA-1/ICAM-1-mediated alteration in TGF-? signaling. LFA-1/ICAM-1-stimulated human and mouse T-cells were refractory to TGF-?-mediated induction of FOXP3(+) (forkhead box P3) and ROR?t(+) (retinoic acid-related orphan nuclear receptor ?t) Th17 differentiation. These mechanistic data suggest an important role for LFA-1/ICAM-1 interactions in immunoregulation concurrent with lymphocyte migration that may have implications at the level of local inflammatory response and for anti-LFA-1-based therapies. PMID:22707713

Verma, Navin K; Dempsey, Eugene; Long, Aideen; Davies, Anthony; Barry, Sean P; Fallon, Padraic G; Volkov, Yuri; Kelleher, Dermot

2012-06-15

150

Carcinoembryonic Antigen-Related Cell Adhesion Molecule 1 Inhibits MMP-9-Mediated Blood-Brain-Barrier Breakdown in a Mouse Model for Ischemic Stroke.  

PubMed

Rationale: Blood-brain-barrier (BBB) breakdown and cerebral edema result from postischemic inflammation and contribute to mortality and morbidity after ischemic stroke. A functional role for the carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) in the regulation of reperfusion injury has not yet been demonstrated. Objective: We sought to identify and characterize the relevance of CEACAM1-expressing inflammatory cells in BBB breakdown and outcome after ischemic stroke in Ceacam1(-/-) and wild-type mice. Methods and Results: Focal ischemia was induced by temporary occlusion of the middle cerebral artery with a microfilament. Using MRI and Evans blue permeability assays, we observed increased stroke volumes, BBB breakdown and edema formation, reduction of cerebral perfusion, and brain atrophy in Ceacam1(-/-) mice. This translated into poor performance in neurological scoring and high poststroke-associated mortality. Elevated neutrophil influx, hyperproduction, and release of neutrophil-related matrix metalloproteinase-9 in Ceacam1(-/-) mice were confirmed by immune fluorescence, flow cytometry, zymography, and stimulation of neutrophils. Importantly, neutralization of matrix metalloproteinase-9 activity in Ceacam1(-/-) mice was sufficient to alleviate stroke sizes and improve survival to the level of CEACAM1-competent animals. Immune histochemistry of murine and human poststroke autoptic brains congruently identified abundance of CEACAM1(+)matrix metalloproteinase-9(+) neutrophils in the ischemic hemispheres. Conclusions: CEACAM1 controls matrix metalloproteinase-9 secretion by neutrophils in postischemic inflammation at the BBB after stroke. We propose CEACAM1 as an important inhibitory regulator of neutrophil-mediated tissue damage and BBB breakdown in focal cerebral ischemia. PMID:23780386

Ludewig, Peter; Sedlacik, Jan; Gelderblom, Mathias; Bernreuther, Christian; Korkusuz, Yücel; Wagener, Christoph; Gerloff, Christian; Fiehler, Jens; Magnus, Tim; Horst, Andrea Kristina

2013-06-18

151

Sexual size dimorphism predicts rates of sequence evolution of SPerm Adhesion Molecule 1 (SPAM1, also PH-20) in monkeys, but not in hominoids (apes including humans).  

PubMed

Based on a dataset comprising coding DNA sequences of 23 anthropoid primates, we herein investigate if rates of sequence evolution of SPerm Adhesion Molecule1 (SPAM1, also PH-20), which participates in sperm-egg interaction, is lower in more sexually dimorphic species. For comparison, we analyze sequence evolution of apolipoproteinA-IV (APOA4) and apolipoprotein A-V (APOA5), which should evolve under less or even no sexual selection given their expression in blood, digestive tract, liver, and lungs. Regression analyses provides significant support for a negative dependence of SPAM1 derived branch-specific ratios of non-synonymous to synonymous substitution rates (dN/dS) on sexual size dimorphism (SSD) in a subsample comprising New World and Old World monkeys. We moreover observed a tendency for a positive correlation of substitution rates of SPAM1 with relative testes weight (RTW) and significantly lowered dN/dS estimates in uni-male and uni-male/multi-male breeding monkeys. Importantly, the pattern was not reproduced when analyzing partial APOA4 and APOA5 sequences. These findings illustrate that different levels of sperm competition, probably fueled by female cryptic choice, account for species-specific sequence evolution of SPAM1 in monkeys. Remarkably, present data do not support a correlation of species-specific sequence evolution of SPAM1 with sexual selection levels in hominoids (apes including humans). This can partly be ascribed to a relaxation of functional constraint of SPAM1 in some hominoid species. Additional factors confounding regression analyses specifically in hominoids might be higher levels of sperm competition than reflected by SSD and RTW in some species, a rather strong effect of female mate choice on paternity rates in others, and - in particular in humans - socio-cultural factors not measurable by SSD and RTW. PMID:22197807

Prothmann, Andreas; Laube, Irina; Dietz, Johanna; Roos, Christian; Mengel, Katja; Zischler, Hans; Herlyn, Holger

2011-12-14

152

Leukocyte Function-associated Antigen-1/Intercellular Adhesion Molecule-1 Interaction Induces a Novel Genetic Signature Resulting in T-cells Refractory to Transforming Growth Factor-? Signaling*  

PubMed Central

The immunesuppressive cytokine TGF-? plays crucial regulatory roles in the induction and maintenance of immunologic tolerance and prevention of immunopathologies. However, it remains unclear how circulating T-cells can escape from the quiescent state maintained by TGF-?. Here, we report that the T-cell integrin leukocyte function-associated antigen-1 (LFA-1) interaction with its ligand intercellular adhesion molecule-1 (ICAM-1) induces a genetic signature associated with reduced TGF-? responsiveness via up-regulation of SKI, E3 ubiquitin-protein ligase SMURF2, and SMAD7 (mothers against decapentaplegic homolog 7) genes and proteins. We confirmed that the expression of these TGF-? inhibitory molecules was dependent on STAT3 and/or JNK activation. Increased expression of SMAD7 and SMURF2 in LFA-1/ICAM-1 cross-linked T-cells resulted in impaired TGF-?-mediated phosphorylation of SMAD2 and suppression of IL-2 secretion. Expression of SKI caused resistance to TGF-?-mediated suppression of IL-2, but SMAD2 phosphorylation was unaffected. Blocking LFA-1 by neutralizing antibody or specific knockdown of TGF-? inhibitory molecules by siRNA substantially restored LFA-1/ICAM-1-mediated alteration in TGF-? signaling. LFA-1/ICAM-1-stimulated human and mouse T-cells were refractory to TGF-?-mediated induction of FOXP3+ (forkhead box P3) and ROR?t+ (retinoic acid-related orphan nuclear receptor ?t) Th17 differentiation. These mechanistic data suggest an important role for LFA-1/ICAM-1 interactions in immunoregulation concurrent with lymphocyte migration that may have implications at the level of local inflammatory response and for anti-LFA-1-based therapies.

Verma, Navin K.; Dempsey, Eugene; Long, Aideen; Davies, Anthony; Barry, Sean P.; Fallon, Padraic G.; Volkov, Yuri; Kelleher, Dermot

2012-01-01

153

Human T-cell lymphotropic virus type 1 (HTLV-1)-induced syncytium formation mediated by vascular cell adhesion molecule-1: evidence for involvement of cell adhesion molecules in HTLV-1 biology.  

PubMed Central

While studying the potential role of vascular cell adhesion molecule-1 (VCAM-1) in infection of endothelial cells by human immunodeficiency virus (HIV), we found that VCAM-1 can mediate human T-cell lymphotropic virus type 1 (HTLV-1)-induced syncytium formation. Both expression-vector-encoded and endogenously expressed VCAM-1 supported fusion of uninfected cells with HTLV-1-infected cells. Fusion was obtained with cell lines carrying the HTLV-1 genome and expressing viral proteins but not with an HTLV-1-transformed cell line that does not express viral proteins. In clones of VCAM-1-transfected cells, the degree of syncytium formation observed directly reflected the level of VCAM-1 expression. Syncytium formation between HTLV-1-expressing cells and VCAM-1+ cells could be blocked with antiserum against HTLV-1 gp46 and with a monoclonal antibody (MAb) against VCAM-1. Fusion was not blocked by antiserum against HIV or a MAb against VLA-4, the physiological counter-receptor for VCAM-1. The results indicate that VCAM-1 can serve as an accessory molecule or potential coreceptor for HTLV-1-induced cell fusion and provide direct evidence of a role for cell adhesion molecules in the biology of HTLV-1.

Hildreth, J E; Subramanium, A; Hampton, R A

1997-01-01

154

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

155

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

156

The direct effect of injectable cyclosporine and its vehicle, cremophor, on endothelial vascular cell adhesion molecule-1 expression. Ricinoleic acid inhibits coronary artery endothelial activation.  

PubMed

As in humans, rabbit coronary artery endothelium basally expresses vascular cell adhesion molecule-1 (VCAM-1). Treatment with parenteral cyclosporine (CsA) to prevent graft rejection in rabbits receiving heterotopic heart transplantation reduced VCAM-1 expression in coronary arteries not only in transplanted, but also in native rabbit hearts. To explore the mechanism of this effect, we co-incubated cultured human saphenous vein endothelial cells for 24 hr with CsA or its vehicle (containing polyoxyethylated castor oil, or Cremophor, and ethanol), at concentrations compatible with those achievable in plasma during administration of parenteral preparations of CsA. Cells were then stimulated with TNF alpha or IL-4 to induce VCAM-1 expression, assessed by a cell-surface enzyme immunoassay. Both CsA and vehicle inhibited IL-4-stimulated VCAM-1 expression in a dose-dependent manner (from [OD mU, mean +/- SEM] 230 +/- 5 to 165 +/- 3 for CsA 50 ng/ml, and to 181 +/- 6 for the corresponding vehicle concentration; P < 0.05 for both comparisons). To investigate whether this vehicle effect also occurs in vivo, we treated 9 New Zealand White rabbits with saline (n = 3), CsA (10 mg/kg/day, n = 3), or vehicle at corresponding doses (n = 3) for 6 weeks. Profiles of coronary arteries (> or = 48 for each group) were semiquantitatively scored (0-5) for VCAM-1 in immunostained heart cross-sections. Administration of both CsA and vehicle significantly reduced VCAM-1 expression compared with saline. Two vehicle components, ethanol and ricinoleic acid, were further evaluated directly on endothelial cells in vitro. While ethanol was ineffective, the monounsaturated fatty acid ricinoleic acid inhibited IL-4-stimulated VCAM-1 expression in a dose-dependent manner (IC50 between 10 and 100 microM). Thus, a fatty acid component of CsA vehicle exerts direct endothelial effects, potentially limiting arterial leukocyte recruitment during parenteral CsA treatment. This observation reveals a novel mechanism for CsA as an inhibitor of leukocyte-endothelial interactions, and furnishes a new potential rationale for the therapeutic action of unsaturated fatty acids in graft coronary disease. PMID:7544037

De Caterina, R; Tanaka, H; Nakagawa, T; Hauptman, P J; Libby, P

1995-08-15

157

A Carcinoembryonic Antigen-Related Cell Adhesion Molecule 1 Homologue Plays a Pivotal Role in Nontypeable Haemophilus influenzae Colonization of the Chinchilla Nasopharynx via the Outer Membrane Protein P5Homologous Adhesin  

Microsoft Academic Search

In vitro studies suggest an important role for CEACAM1 (carcinoembryonic antigen-related cell adhesion molecule 1) in infection by multiple gram-negative bacteria. However, in vivo evidence supporting this role is lacking, largely because the bacterial adhesins involved in this host-microbe association do not bind to murine-derived CEACAM1. One of several adhesins expressed by nontypeable Haemophilus influenzae (NTHI), the outer membrane protein

James E. Bookwalter; Joseph A. Jurcisek; Scott D. Gray-Owen; Soledad Fernandez; Glen McGillivary; Lauren O. Bakaletz

2008-01-01

158

L-selectin and intercellular adhesion molecule 1 mediate lymphocyte migration to the inflamed airway\\/lung during an allergic inflammatory response in an animal model of asthma  

Microsoft Academic Search

T lymphocytes play a critical role in the development of allergic inflammation in asthma. Early in the allergic response, T lymphocytes migrate from the circulation into the lung to initiate and propagate airway inflammation. The adhesion molecules that mediate lymphocyte entry into inflamed lung have not been defined. This study directly examined the roles of L-selectin and intercellular adhesion molecule

Efthimia Keramidaris; Toby D. Merson; Douglas A. Steeber; Thomas F. Tedder; Mimi L. K. Tang

2001-01-01

159

Transient Variations in the Serum Concentrations of Cell Adhesion Molecules Following Retroperitoneal Laparoscopic and Open Radical Nephrectomy for Localized Renal-Cell Carcinoma  

PubMed Central

Abstract Purpose To evaluate differences in the serum concentrations of cell adhesion molecules (CAMs) after retroperitoneal laparoscopic and conventional open radical nephrectomies for localized renal-cell carcinoma (RCC). Patients and Methods A total of 62 patients with stage T1N0M0 RCC were randomized to either a retroperitoneal laparoscopic radical nephrectomy group (n=31) or an open group (n=31). Serum levels of soluble cluster of differentiation 44 splice variant 6 (sCD44v6), soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), and soluble epithelial cadherin (sE-cadherin) were determined independently by enzyme linked immunosorbent assay (ELISA) preoperatively, and on postoperative days 1 and 5. In addition, follow-up results were compared. Results On postoperative day 1, sCD44v6, sICAM-1, and sVCAM-1 levels increased significantly compared with preoperative levels in both groups (P<0.05). sE-cadherin levels decreased compared with preoperative levels in both groups without statistically significant differences (P>0.05). sCD44v6 levels in the retro-laparoscopy group were significantly higher than in the open group (P<0.05), while sICAM-1, sVCAM-1, and sE-cadherin levels showed no statistically significant differences between both groups (P>0.05). On postoperative day 5, all parameters in both groups were similar to preoperative values (P>0.05). Follow-up ranged from 7 to 18 months postoperatively in all 62 patients, with a 100% cancer-specific survival rate in each group. Conclusion Although postoperatively higher serum concentrations of CAMs in both groups and significantly elevated sCD44v6 in the retro-laparoscopy group may be facilitated, the differences in CAMs between both groups are small and transient. Together with the similar follow-up results, this further supports previous studies that failed to show a difference in the oncologic outcomes between open and laparoscopic radical nephrectomy and provides a probable molecular mechanism.

Yang, Lu; Wei, Qiang; Cui, Xiaobo; Bu, Siyuan; Han, Ping

2012-01-01

160

Coordinated but depressed expression of human leukocyte antigen-DR, intercellular adhesion molecule-1, and CD14 on peritoneal macrophages in women with pelvic endometriosis  

Microsoft Academic Search

ObjectiveTo investigate the macrophage response in endometriosis, we determined the expression of human leukocyte antigen (HLA)-DR, intercellular adhesion molecule (ICAM)-1, and CD14 on peritoneal macrophages.

Chiaki Izumiya; Nagamasa Maeda; Tomoaki Kusume; Takayuki Masumoto; Chika Yamashita; Yorito Yamamoto; Hiroyoshi Oguri; Takao Fukaya

2003-01-01

161

Vascular cell adhesion molecule-1 expression in human intestinal microvascular endothelial cells is regulated by PI 3-kinase/Akt/MAPK/NF-kappaB: inhibitory role of curcumin.  

PubMed

Endothelial activation and surface expression of cell adhesion molecules (CAMs) is critical for binding and recruitment of circulating leukocytes in tissues during the inflammatory response. Endothelial CAM expression plays a critical role in the intestinal microvasculature in inflammatory bowel disease (IBD), as blockade of leukocyte alpha4-integrin binding by gut endothelial CAM ligands has therapeutic benefit in IBD. Mechanisms underlying expression of vascular cell adhesion molecule (VCAM)-1, a ligand for alpha4-integrin in primary cultures of human intestinal microvascular endothelial cells (HIMEC) has not been defined. We investigated the effect of curcumin, phosphatidylinositol 3-kinase (PI 3-kinase)/protein kinase B (Akt), and mitogen-activated protein kinase (MAPK) inhibitors on VCAM-1 expression and function in HIMEC. CAM expression was assessed and HIMEC-leukocyte adhesion was visualized under static and flow conditions. Western blotting and in vitro kinase assays were used to assess Akt and MAPK activation. Nuclear factor-kappaB (NF-kappaB) activation and nuclear translocation of its p65 subunit were determined. Tumor necrosis factor (TNF)-alpha/lipopolysaccharide (LPS)-induced VCAM-1 expression in HIMEC was suppressed by Akt small-interfering RNA, curcumin, and inhibitors of NF-kappaB (SN-50), p38 MAPK (SB-203580) and PI 3-kinase/Akt (LY-294002). VCAM-1 induction was partially suppressed by p44/42 MAPK (PD-098059) but unaffected by c-Jun NH2-terminal kinase (SP-600125) inhibition. Curcumin inhibited Akt/MAPK/NF-kappaB activity and prevented nuclear translocation of the p65 NF-kappaB subunit following TNF-alpha/LPS. At physiological shear stress, curcumin attenuated leukocyte adhesion to TNF-alpha/LPS-activated HIMEC monolayers. In conclusion, curcumin inhibited the expression of VCAM-1 in HIMECs through blockade of Akt, p38 MAPK, and NF-kappaB. Curcumin may represent a novel therapeutic agent targeting endothelial activation in IBD. PMID:19520742

Binion, David G; Heidemann, Jan; Li, Mona S; Nelson, Victoria M; Otterson, Mary F; Rafiee, Parvaneh

2009-06-11

162

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

163

Mediation by NF-?B of cytokine induced expression of intercellular adhesion molecule 1 (ICAM-1) in an intestinal epithelial cell line, a process blocked by proteasome inhibitors  

Microsoft Academic Search

Background\\/aims—The gene promoter for the intercellular adhesion molecule ICAM-1 possesses binding sites for several transcriptional factors, including nuclear factor ?B (NF-?B). The role of NF-?B in ICAM-1 gene regulation was therefore examined by using different proteasome inhibitors in tumour necrosis factor ? (TNF-?) stimulated IEC-6 rat intestinal epithelial cells.Methods—ICAM-1 expression was analysed by enzyme linked immunosorbent assay (ELISA), reverse transcriptase

C Jobin; C Hellerbrand; L L Licato; D A Brenner; R B Sartor

1998-01-01

164

N-acetyl-D-galactosamine specific lectin of Eikenella corrodens induces intercellular adhesion molecule-1 (ICAM-1) production by human oral epithelial cells.  

PubMed

During the acute inflammatory response in periodontitis, gingival epithelial cells are considered to play important roles in the recruitment of inflammatory cells to the site of infection through the secretion of chemokines. However, little is known about the expression of molecules that are involved in the interaction between the epithelium and neutrophils following bacterial attachment. Earlier work reported that periodontopathogenic Eikenella corrodens strain 1,073 up-regulated the expression and secretion of chemokines such as interleukin-8 (IL-8) from KB cells (a human oral epithelial cell line derived from a human oral epidermoid carcinoma). To elucidate the mechanism of the transmigration of neutrophils through the epithelium, the present study investigated the expression of adhesion molecules on KB cells in response to E. corrodens attachment. Adhesion molecule gene expression was assessed by RT-PCR and adhesion proteins expressed on KB cell surfaces were determined by cell-based ELISA and FACS. In RT-PCR, ICAM-1 mRNA levels were significantly increased within 1 h in response to exposure to E. corrodens and continued to increase over the 12-h period of study. In ELISA, increased surface ICAM-1 expression was paralleled by increased ICAM-1 mRNA levels. Furthermore, the increases in ICAM-1 expression on epithelial cells infected with E. corrodens were observed to be due to the N-acetyl-D-galactosamine (GalNAc) specific bacterial lectin-like substance of E. corrodens (EcLS), which was one of the adhesins of E. corrodens. This is the first study to report that a bacterial lectin-like substance increased the expression of ICAM-1 on gingival epithelial cells. PMID:12466406

Yamada, Masayoshi; Nakae, Hideaki; Yumoto, Hiromichi; Shinohara, Chihiro; Ebisu, Shigeyuki; Matsuo, Takashi

2002-12-01

165

Costimulation by purified intercellular adhesion molecule 1 and lymphocyte function-associated antigen 3 induces distinct proliferation, cytokine and cell surface antigen profiles in human "naive" and "memory" CD4+ T cells  

PubMed Central

Activation of resting human CD4+ "naive" (CD45RA+CD45RO-) and "memory" (CD45RA-CD45RO+) T cells requires costimulatory signals in addition to engagement of the T cell receptor/CD3 complex (TCR/CD3). The adhesion pathways mediated by lymphocyte function-associated antigen 1/intercellular adhesion molecule 1 (LFA-1/ICAM-1) and CD2/LFA-3 are capable of providing such costimulatory signals. Our work shows that these costimulatory adhesion pathways are critically involved in regulation of T cell differentiation/maturation. Evidence for subset- specific costimulatory requirements is demonstrated by the finding that only memory CD4+ T cells were costimulated by LFA-3, whereas both naive and memory CD4+ T cells were costimulated by ICAM-1. In addition, these costimulatory adhesion pathways regulated reciprocal cytokine secretion patterns for interleukin 5 (IL-5) and granulocyte/macrophage colony- stimulating factor (GM-CSF). Repeated costimulation of CD4+ memory T cells with LFA-3 led to secretion of high levels of IL-5, while repeated costimulation with ICAM-1 induced high levels of secreted GM- CSF. Significant interferon gamma (IFN-gamma) production was observed with either of the costimulatory ligands. Extensive cell surface analysis of these in vitro cultures of peripheral blood derived memory CD4+ T cells, with monoclonal antibodies obtained from the 5th Leucocyte Typing Workshop, revealed differential expression of a singular antigen, CD60. This antigen was preferentially expressed on LFA-3-costimulated cells suggesting a positive correlation between CD60 expression and a T helper type 2-like cytokine profile. In conclusion, this report demonstrates a new functional role for costimulatory adhesion molecules in regulating differential cytokine secretion in human memory CD4+ T cells.

1994-01-01

166

Effects of anti-tumor necrosis factor-alpha and anti-intercellular adhesion molecule-1 antibodies on ischemia/reperfusion lung injury.  

PubMed

Inhibition of neutrophil activation and adherence to endothelium by antibodies to tumor necrosis factor-alpha (TNF-alpha) and intercellular adhesion molecules (ICAM-1), respectively, might attenuate ischemia-reperfusion injury (I/R). I/R was conducted in an isolated rat lung model. Anti-TNF-alpha antibody and/or anti-ICAM-1 antibody were added before ischemia or after reperfusion. Hemodynamic changes, lung weight gain (LWG), capillary filtration coefficients (Kfc), and pathologic changes were assessed to evaluate the severity of I/R. The LWG, Kfc, pathological changes and lung injury score of treatment groups with anti-TNF-alpha antibody treatment, either pre-ischemia or during reperfusion, were less than those observed in control groups. Similar findings were found in group treated with anti-ICAM-1 antibody or combination therapy during reperfusion. In contrast, pre-I/R treatment with anti-ICAM-1 antibody induced severe lung edema and failure to complete the experimental procedure. No additional therapeutic effect was found in combination therapy. We conclude that TNF-alpha and ICAM-1 play important roles in I/R. Anti-TNF-alpha antibody has therapeutic and preventive effects on I/R. However, combined therapy with anti-TNF-alpha antibody and anti-ICAM-1 antibody may have no additive effect and need further investigation. PMID:17294835

Chiang, Chi-Huei

2006-10-31

167

Expression of leucocyte function-associated antigen-1 and intercellular adhesion molecule-1 in the lungs of pigs infected with Actinobacillus pleuropneumoniae.  

PubMed

The aim of this study was to determine the expression of leucocyte function-associated antigen (LFA)-1 (CD11a/CD18) by neutrophils and intercellular adhesion molecule (ICAM)-1 (CD54) by endothelial cells in the lungs of pigs that had been infected experimentally with Actinobacillus pleuropneumoniae. Sixty-four 7-week-old conventional pigs were allocated randomly into infected (n = 40) or control (n = 24) groups. Five infected and three uninfected pigs were killed at 3, 6, 9, 12, 24, 36, 48 and 60 h post inoculation (hpi). Strong immunohistochemical expression of LFA-1 and ICAM-1 was detected frequently in neutrophils in the alveolar space and in endothelial cells in the capillaries of the alveolar septa, respectively. LFA-1 and ICAM-1 expression appeared to correlate with the onset of neutrophil infiltration into the alveolar space. The interaction between ICAM-1 and LFA-1 may be associated with the adherence of neutrophils to vascular endothelium, thereby permitting transmigration of these cells into inflamed lung. PMID:22819014

Oh, Y; Ha, Y; Han, K; Seo, H W; Kang, I; Park, C; Kim, S C; Kim, S-H; Chae, C

2012-07-20

168

Interleukin-17 synergizes with IFN? or TNF? to promote inflammatory mediator release and intercellular adhesion molecule-1 (ICAM-1) expression in human intervertebral disc cells  

PubMed Central

Interleukin-17 (IL-17) is a cytokine recently shown to be elevated, along with interferon-? (IFN?) and tumor necrosis factor (TNF?), in degenerated and herniated intervertebral disc (IVD) tissues, suggesting a role for these cytokines in intervertebral disc disease. The objective of our study was to investigate the involvement of IL-17 and costimulants IFN? and TNF? in intervertebral disc pathology. Cells were isolated from anulus fibrosus and nucleus pulposus tissues of patients undergoing surgery for intervertebral disc degeneration or scoliosis. The production of inflammatory mediators, nitric oxide (NOx), prostaglandin E2 (PGE2) and interleukin-6 (IL-6), as well as intercellular adhesion molecule (ICAM-1) expression, were quantified for cultured cells following exposure to IL-17, IFN? and TNF?. Intervertebral disc cells exposed to IL-17, IFN? or TNF? showed a remarkable increase in inflammatory mediator release and ICAM-1 expression (GLM and ANOVA, p<0.05). Addition of IFN? or TNF? to IL-17 demonstrated a synergistic increase in inflammatory mediator release, and a marked increase in ICAM-1 expression. These findings suggest that IVD cells not only respond with a catabolic phenotype to IL-17 and costimulants IFN? and TNF?, but also express surface ligands with consequent potential to recruit additional lymphocytes and immune cells to the IVD microenvironment. IL-17 may be an important regulator of inflammation in the IVD pathologies.

Gabr, Mostafa A.; Jing, Liufang; Helbling, Antonia R.; Sinclair, S. Michael; Allen, Kyle D.; Shamji, Mohammed F.; Richardson, William J.; Fitch, Robert D.; Setton, Lori A.; Chen, Jun

2010-01-01

169

Hypoxic stress alone does not modulate endothelial surface expression of bovine E-selectin and intercellular adhesion molecule-1 (ICAM-1).  

PubMed

Hypoxemia is a common event in many vascular diseases, especially vascular ischemia. Since endothelial cells of blood vessels are exposed to conditions within the vascular space and leucocytes play a key role in ischemia/reperfusion injury, we hypothesized that endothelial exposure to hypoxia may regulate expression of surface proteins important in leucocyte-endothelial interactions, such as E-selectin and intercellular adhesion molecule (ICAM-1). In this study, we used isolated bovine aortic endothelial monolayers to examine endothelial surface alterations of E-selectin and ICAM-1 induced by tumor necrosis factor-alpha (TNF-alpha), lipopolysaccharide (LPS) and hypoxia using a whole cell enzyme-linked immunosorbent assay (ELISA). Bovine endothelial exposure to TNF-alpha (50 ng/mL) induced a time dependent increase (range 0-24h) in specific E-selection surface expression. Endothelial exposure to hypoxia alone (pO2 approximately 3 mmHg, range 0-24 h), however, failed to elicit endothelial E-selectin expression. Endothelial exposure to LPS brought about a dose- and time-dependent (range 0.5 ng/mL and 2-8 h) increase in specific ICAM-1 surface expression (max. 3.5 +/- 0.15-fold increase over no cytokine control at 10 ng/mL, 4 h). Hypoxia (pO2 approximately 3 mmHg, 8h), however, did not induce ICAM-1 surface expression over normoxia levels. In conclusion: i) bovine endothelial E-selectin and ICAM-1 surface expression are regulated molecules, ii) hypoxia, per se, does not regulate surface expression of either E-selectin or ICAM-1. These results suggest that hypoxic endothelia may require additional external signals for generation of adaptive inflammatory responses. PMID:8653575

Zünd, G; Dzus, A L; McGuirk, D K; Breuer, C; Shinoka, T; Mayer, J E; Colgan, S P

1996-01-01

170

Reduced Expression of Adipose Triglyceride Lipase Enhances Tumor Necrosis Factor ?-induced Intercellular Adhesion Molecule-1 Expression in Human Aortic Endothelial Cells via Protein Kinase C-dependent Activation of Nuclear Factor-?B*  

PubMed Central

We examined the effects of adipose triglyceride lipase (ATGL) on the initiation of atherosclerosis. ATGL was recently identified as a rate-limiting triglyceride (TG) lipase. Mutations in the human ATGL gene are associated with neutral lipid storage disease with myopathy, a rare genetic disease characterized by excessive accumulation of TG in multiple tissues. The cardiac phenotype, known as triglyceride deposit cardiomyovasculopathy, shows massive TG accumulation in both coronary atherosclerotic lesions and the myocardium. Recent reports show that myocardial triglyceride content is significantly higher in patients with prediabetes or diabetes and that ATGL expression is decreased in the obese insulin-resistant state. Therefore, we investigated the effect of decreased ATGL activity on the development of atherosclerosis using human aortic endothelial cells. We found that ATGL knockdown enhanced monocyte adhesion via increased expression of TNF?-induced intercellular adhesion molecule-1 (ICAM-1). Next, we determined the pathways (MAPK, PKC, or NF?B) involved in ICAM-1 up-regulation induced by ATGL knockdown. Both phosphorylation of PKC and degradation of I?B? were increased in ATGL knockdown human aortic endothelial cells. In addition, intracellular diacylglycerol levels and free fatty acid uptake via CD36 were significantly increased in these cells. Inhibition of the PKC pathway using calphostin C and GF109203X suppressed TNF?-induced ICAM-1 expression. In conclusion, we showed that ATGL knockdown increased monocyte adhesion to the endothelium through enhanced TNF?-induced ICAM-1 expression via activation of NF?B and PKC. These results suggest that reduced ATGL expression may influence the atherogenic process in neutral lipid storage diseases and in the insulin-resistant state.

Inoue, Tomoaki; Kobayashi, Kunihisa; Inoguchi, Toyoshi; Sonoda, Noriyuki; Fujii, Masakazu; Maeda, Yasutaka; Fujimura, Yoshinori; Miura, Daisuke; Hirano, Ken-ichi; Takayanagi, Ryoichi

2011-01-01

171

Different intrathyroid expression of intercellular adhesion molecule-1 (ICAM-1) in Hashimoto's thyroiditis and Graves' disease: analysis at mRNA level and association with B7.1 costimulatory molecule.  

PubMed

Cultured thyroid epithelial cells can be induced to express intercellular adhesion molecule-1 (ICAM-1, or CD54). However, constitutive follicular expression of ICAM-1 has been reported only in thyroid autoimmunity. We evaluated the expression of ICAM-1 mRNA and protein on thyroid tissue from different autoimmune thyroid diseases, and its relationship with other immunologically relevant surface markers, namely costimulatory molecules of B7 family. Thyroid tissue sections were obtained by surgically removed thyroid glands from 6 patients with Hashimoto's thyroiditis (HT), 6 with Graves' disease (GD) and 3 with multinodular nontoxic goiter. We used in situ hybridization to localize ICAM-1 mRNA, and immunohistochemical analysis by alkaline phosphatase anti-alkaline phosphatase (APAAP) method. We showed a clear hybridization pattern, localized in follicular cells, in sections of glands with HT. The hybridization pattern was far less pronounced in GD: no staining was apparent on follicular cells. These results were strictly consistent with those obtained by means of immunohistochemistry. Moreover, double-staining experiments demonstrated colocalization of ICAM-1 and B7.1 molecules in HT, whereas no B7.1 expression was observed in Graves' or in non-autoimmune thyroid diseases. These data agree with the hypothesis of distinct immunoregulatory phenomena and effector mechanisms in the 2 main autoimmune thyroid diseases. PMID:11936473

Pesce, G; Fiorino, N; Riccio, A M; Montagna, P; Torre, G; Salmaso, C; Altrinetti, V; Bagnasco, M

2002-03-01

172

Anthocyanins from purple sweet potato Ipomoea batatas cultivar Ayamurasaki suppress the development of atherosclerotic lesions and both enhancements of oxidative stress and soluble vascular cell adhesion molecule-1 in apolipoprotein E-deficient mice.  

PubMed

We evaluated the protective potential of anthocyanins from purple sweet potato Ipomoea batatas cultivar Ayamurasaki (APSP) against low-density lipoprotein (LDL) oxidation in vitro and atherosclerotic lesion development in apolipoprotein E-deficient mice given a cholesterol- and fat-enriched diet with or without 1% APSP for 4 weeks. APSP protected LDL against oxidation more potently than other anthocyanins and l-ascorbic acid in vitro. In mice, APSP significantly lowered the atherosclerotic plaque area to about half of the control, the liver level of thiobarbituric acid-reactive substances as an oxidative stress marker, and the plasma level of soluble vascular cell adhesion molecule-1 (sVCAM-1). However, APSP showed no effects on body weight and cholesterol and lipid levels in the plasma. The results suggest that APSP can suppress the development of atherosclerotic lesions and both enhancements of oxidative stress and sVCAM-1 independently of the changes in cholesterol and lipid levels in mice. PMID:18986148

Miyazaki, Kouji; Makino, Kumiko; Iwadate, Emi; Deguchi, Yoriko; Ishikawa, Fumiyasu

2008-12-10

173

Small GTPase Rho signaling is involved in {beta}1 integrin-mediated up-regulation of intercellular adhesion molecule 1 and receptor activator of nuclear factor {kappa}B ligand on osteoblasts and osteoclast maturation  

SciTech Connect

We assessed the characteristics of human osteoblasts, focusing on small GTPase Rho signaling. {beta}1 Integrin were highly expressed on osteoblasts. Engagement of {beta}1 integrins by type I collagen augmented expression of intercellular adhesion molecule 1 (ICAM-1) and receptor activator of nuclear factor {kappa}B ligand (RANKL) on osteoblasts. Rho was activated by {beta}1 stimulation in osteoblasts. {beta}1 Integrin-induced up-regulation of ICAM-1 and RANKL was inhibited by transfection with adenoviruses encoding C3 transferase or pretreated with Y-27632, specific Rho and Rho-kinase inhibitors. Engagement of {beta}1 integrin on osteoblasts induced formation of tartrate-resistant acid phosphatase (TRAP)-positive multinuclear cells (MNC) in a coculture system of osteoblasts and peripheral monocytes, but this action was completely abrogated by transfection of C3 transferase. Our results indicate the direct involvement of Rho-mediated signaling in {beta}1 integrin-induced up-regulation of ICAM-1 and RANKL and RANKL-dependent osteoclast maturation. Thus, Rho-mediated signaling in osteoblasts seems to introduce major biases to bone resorption.

Hirai, Fumihiko [First Department of Internal Medicine, University of Occupational and Environmental Health, School of Medicine, Kitakyushu 807-8555 (Japan); Nakayamada, Shingo [First Department of Internal Medicine, University of Occupational and Environmental Health, School of Medicine, Kitakyushu 807-8555 (Japan); Okada, Yosuke [First Department of Internal Medicine, University of Occupational and Environmental Health, School of Medicine, Kitakyushu 807-8555 (Japan); Saito, Kazuyoshi [First Department of Internal Medicine, University of Occupational and Environmental Health, School of Medicine, Kitakyushu 807-8555 (Japan); Kurose, Hitoshi [Department of Pharmacology and Toxicology, Graduate School of Pharmaceutical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582 (Japan); Mogami, Akira [Pharmaceuticals Research Unit Research and Development Division Mitsubishi Pharma Corporation, Kamoshida-cho, Aoba-ku, Yokohama 227-0033 (Japan); Tanaka, Yoshiya [First Department of Internal Medicine, University of Occupational and Environmental Health, School of Medicine, Kitakyushu 807-8555 (Japan)]. E-mail: tanaka@med.uoeh-u.ac.jp

2007-04-27

174

Vascular endothelial growth factor participates in modulating the C6 glioma-induced migration of rat bone marrow-derived mesenchymal stem cells and upregulates their vascular cell adhesion molecule-1 expression.  

PubMed

Bone marrow-derived mesenchymal stem cells (BMSCs) have been shown to be able to migrate towards glioma, but the molecular mechanisms responsible for this migratory behavior still require further elucidation. This study aimed to test the role of vascular endothelial growth factor (VEGF) in the C6 glioma-induced migration of BMSCs, evaluate the effect of VEGF on the migratory capacity and vascular cell adhesion molecule-1 (VCAM-1) expression of BMSCs and explore the role of VCAM-1 in the VEGF-induced migration of BMSCs. The results showed that C6 glioma cells significantly increased the migration of BMSCs in vitro, which was partially blocked by a VEGF neutralizing antibody, and 20 ng/ml recombinant rat VEGF(164) incubation enhanced the migration of BMSCs. Moreover, 12 h of 20 ng/ml VEGF(164) incubation upregulated the VCAM-1 expression of BMSCs and the blocking of VCAM-1 reduced the VEGF(164)-induced migration of BMSCs. The data also revealed that LY294002, an inhibitor of phosphoinositide-3-kinase (PI3K), decreased the VEGF-induced migration and VCAM-1 expression of BMSCs. These findings indicate that VEGF participates in mediating the C6 glioma-induced migration of BMSCs by upregulating their VCAM-1 expression, and that PI3K is involved in the signal transduction of VEGF(164)-induced migration and VCAM-1 expression of BMSCs. PMID:23226762

Gao, Zhiqiang; Cheng, Peng; Xue, Yixue; Liu, Yunhui

2012-09-14

175

Hypoxia-inducible factor 1 alpha-activated angiopoietin-like protein 4 contributes to tumor metastasis via vascular cell adhesion molecule-1/integrin ?1 signaling in human hepatocellular carcinoma.  

PubMed

Angiopoietin-like protein 4 (ANGPTL4) plays complex and often contradictory roles in vascular biology and tumor metastasis, but little is known about its function in hepatocellular carcinoma (HCC) metastasis. In the present study, we showed that hypoxia-inducible factor 1? (HIF-1?) directly up-regulates ANGPTL4, and its stableness positively correlates with ANGPTL4 expression in HCC tissue. Overexpression of ANGPTL4 significantly increased HCC cell transendothelial migration in vitro and intrahepatic and distal pulmonary metastasis in vivo, whereas silencing ANGPTL4 expression or treatment with a neutralizing antibody specific for ANGPTL4 protein resulted in a reduced transendothelial migration. We also found that serum ANGPTL4 is higher in HCC patients, compared to healthy control, and correlates with intrahepatic metastasis and histological grade. Further, secreted ANGPTL4 promotes transendothelial migration and metastasis of HCC cells in vitro and in vivo through the up-regulation of vascular cell adhesion molecule-1 (VCAM-1) of human umbilical vein endothelial cells and the activation of the VCAM-1/integrin ?1 axis. Conclusion: ANGPTL4 is a target gene of HIF-1? and acts as an important regulator in the metastasis of HCC. Serum ANGPTL4 correlates with tumor progression and metastasis and might be used to indicate prognosis in HCC patients. PMID:21674552

Li, Hong; Ge, Chao; Zhao, Fangyu; Yan, Mingxia; Hu, Chen; Jia, Deshui; Tian, Hua; Zhu, Miaoxin; Chen, Taoyang; Jiang, Guoping; Xie, Haiyang; Cui, Ying; Gu, Jianren; Tu, Hong; He, Xianghuo; Yao, Ming; Liu, Yongzhong; Li, Jinjun

2011-09-01

176

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

177

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

2011-12-13

178

Upregulation of Intercellular Adhesion Molecule 1 and Proinflammatory Cytokines by the Major Surface Proteins of Treponema maltophilum and Treponema lecithinolyticum, the Phylogenetic Group IV Oral Spirochetes Associated with Periodontitis and Endodontic Infections  

PubMed Central

Treponema maltophilum and Treponema lecithinolyticum belong to the group IV oral spirochetes and are associated with endodontic infections, as well as periodontitis. Recently, the genes encoding the major surface proteins (Msps) of these bacteria (MspA and MspTL, respectively) were cloned and sequenced. The amino acid sequences of these proteins showed significant similarity. In this study we analyzed the functional role of these homologous proteins in human monocytic THP-1 cells and primary cultured periodontal ligament (PDL) cells using recombinant proteins. The complete genes encoding MspA and MspTL without the signal sequence were cloned into Escherichia coli by using the expression vector pQE-30. Fusion proteins tagged with N-terminal hexahistidine (recombinant MspA [rMspA] and rMspTL) were obtained, and any possible contamination of the recombinant proteins with E. coli endotoxin was removed by using polymyxin B-agarose. Flow cytometry showed that rMspA and rMspTL upregulated the expression of intercellular adhesion molecule 1 (ICAM-1) in both THP-1 and PDL cells. Expression of proinflammatory cytokines, such as interleukin-6 (IL-6) and IL-8, was also induced significantly in both cell types by the Msps, as determined by reverse transcription-PCR and an enzyme-linked immunosorbent assay, whereas IL-1? synthesis could be detected only in the THP-1 cells. The upregulation of ICAM-1, IL-6, and IL-8 was completely inhibited by pretreating the cells with an NF-?B activation inhibitor, l-1-tosylamido-2-phenylethyl chloromethyl ketone. This suggests involvement of NF-?B activation. The increased ICAM-1 and IL-8 expression in the THP-1 cells obtained with rMsps was not inhibited in the presence of the IL-1 receptor antagonist (IL-1ra), a natural inhibitor of IL-1. Our results show that the Msps of the group IV oral spirochetes may play an important role in amplifying the local immune response by continuous inflammatory cell recruitment and retention at an infection site by stimulation of expression of ICAM-1 and proinflammatory cytokines.

Lee, Sung-Hoon; Kim, Kack-Kyun; Choi, Bong-Kyu

2005-01-01

179

Adhesion  

NASA Astrophysics Data System (ADS)

Adhesion is a highly practical subject in which the vast majority of published work is either chemical in nature, concerned with chemistry that is thought to occur at an adhesive junction or chemistry of adhesives, or essentially mechanical, concerned with the mechanics of testing and failure of adhesive systems. The role of polymer physics in general and de Gennes' work in particular is to discover what happens at the scale of the polymer chain and hence form a bridge between these two approaches. A distinguishing feature of Gennes' work in adhesion is the way he developed simple models that permitted us to see the essential physics of the situation. This is particularly true in his work in viscoelastic effects on toughness (the de Gennes trumpet) where more sophisticated mechanics had been done but the physical situation was obscure. Much of his work was concerned with the effects of connector molecules in toughening an interface in both elastomeric and glassy materials. This work has been extended by a number of authors and forms the basis of our current understanding of the area.

Brown, Hugh

2008-03-01

180

DC-SIGN and SRCL bind glycans of carcinoembryonic antigen (CEA) and CEA-related cell adhesion molecule 1 (CEACAM1): recombinant human glycan-binding receptors as analytical tools  

Microsoft Academic Search

Members of the family of carcinoembryonic antigen (CEA)-related cell adhesion molecules (CEACAMs) belonging to the immunoglobulin (Ig) superfamily are expressed in a variety of normal and malignant human tissues. As components of the cell membrane, these glycoproteins can make contact with adjacent cells. CEACAM1 and CEACAM5 (CEA) express Lewisx (Lex) structures. As shown by mass spectrometry in conjunction with enzymatic

Alexandra Samsen; Valentina Bogoevska; Birgit Klampe; Ana-Maria Bamberger; Lothar Lucka; Andrea K. Horst; Peter Nollau; Christoph Wagener

2010-01-01

181

Adhesion molecules  

PubMed Central

Adhesion molecules are known to -be important components of an active T-cell mediated immune response. Signals generated at a site of inflammation cause circulating T cells to respond by rolling, arrest and then transmigration through the endothelium, all of which are mediated by adhesion molecules. Consequently, strategies have been developed to treat immune disorders with specific antibodies that block the interaction of adhesion molecules. However, the therapeutic effects of such remedies are not always achieved. Our recent investigations have revealed that intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) work together with chemokines to induce immunosuppression mediated by Mesenchymal stem cells (MSCs), thus demonstrating the dual role of adhesion molecules in immune responses. Since MSCs represent an important component of the stromal cells in an inflammatory microenvironment, our findings provide novel information for understanding the regulation of immune responses and for designing new strategies to treat immune disorders.

Ren, Guangwen; Roberts, Arthur I

2011-01-01

182

Reduction of oxidative stress by oral N-acetyl-L-cysteine treatment decreases plasma soluble vascular cell adhesion molecule-1 concentrations in non-obese, non-dyslipidaemic, normotensive, patients with non-insulin-dependent diabetes  

Microsoft Academic Search

Summary   To assess in vivo effects of antioxidants on vascular cell adhesion molecule (VCAM)-1 expression, circulating soluble VCAM-1\\u000a and intraerythrocytic reduced glutathione (GSH) and GSH disulphide (GSSG) concentrations were evaluated in non-insulin-dependent\\u000a diabetic patients without complications (9 men, 6 women, 48 ± 6 years old) before and after 1 month of either oral N-acetyl-L-cysteine (1.200 mg\\/day) or placebo treatments, given

G. De Mattia; M. C. Bravi; O. Laurenti; M. Cassone-Faldetta; A. Proietti; O. De Luca; A. Armiento; C. Ferri

1998-01-01

183

Soluble platelet selectin (sP-selectin) and soluble vascular cell adhesion molecule-1 (sVCAM-1) decrease during therapy with benznidazole in children with indeterminate form of Chagas' disease  

PubMed Central

The immune response against Trypanosoma cruzi infection has been associated with both protection and pathogenesis. Central events in host defence system- and immune-mediated damage are tightly regulated by cell adhesion molecules (CAM). Levels of sP-selectin and sVCAM-1 were measured in sera from 41 children with the indeterminate phase of Chagas' disease. Simultaneously, levels of soluble adhesion molecule were also quantified in Chagas' disease children undergoing specific chemotherapy with benznidazole. Levels of sP-selectin and sVCAM-1 were found to be elevated in children with indeterminate Chagas' disease before aetiologic therapy was started. However, a small group of patients showed sP-selectin and sVCAM-1 levels comparable to those of non-infected children. A positive correlation between levels of sVCAM-1 and sP-selectin in sera from Chagas' disease patients was found. There was a significantly greater decrease in the titres of sP-selectin and sVCAM-1 in those children receiving benznidazole therapy compared with those children receiving placebo. Measurement of soluble adhesion molecules revealed differences in the activation of the immune system in children with the indeterminate form of Chagas' disease. The early decrease of sP-selectin and sVCAM-1 levels after anti-parasitic treatment suggests that these molecules might be valuable indicators of effective parasitologic clearance.

Laucella, S A; Segura, E L; Riarte, A; Sosa, Estani S

1999-01-01

184

Tumor necrosis factor ?-mediated restructuring of the Sertoli cell barrier in vitro involves matrix metalloprotease 9 (MMP9), membrane-bound intercellular adhesion molecule-1 (ICAM-1) and the actin cytoskeleton  

PubMed Central

The mammalian blood-testis barrier (BTB) restructures throughout spermatogenesis, thereby allowing developing germ cells to enter the adluminal compartment of the seminiferous epithelium. Previous studies have shown pro-inflammatory cytokines such as tumor necrosis factor ? (TNF?) and interleukin-1? to be important regulators of Sertoli cell barrier/BTB function in vitro and in vivo. In this study, the effects of TNF? on Sertoli cell barrier function were assessed, with emphasis on changes in proteases and cell adhesion molecules following treatment. By immunoblotting and immunohistochemistry, MMP9 was found to be present in germ cells, localizing by and large to spermatocytes and spermatids in the adult rat testis. Following treatment of Sertoli cells with physiologically relevant consecutive doses of recombinant human TNF? (25 ng/ml), the steady-state levels of active-matrix metalloprotease 9 (MMP9), membrane-bound intercellular adhesion molecule (mICAM-1) and androgen receptor increased significantly. TNF? also downregulated the steady-state level of occludin, in agreement with earlier results that showed TNF? to disrupt Sertoli cell barrier/BTB function. In addition, TNF? affected the filamentous actin cytoskeleton in Sertoli cells, which appeared to be mediated by cortactin, a regulator of actin dynamics. Taken collectively, these findings imply that germ cells may be involved in BTB restructuring via the localized production of TNF?. These results also illustrate that barrier restructuring correlated with an increase in Sertoli cell mICAM-1, suggesting that it may be critical for adhesion as germ cells traverse the “opened” BTB.

Lydka, Marta; Bilinska, Barbara; Cheng, C. Yan; Mruk, Dolores D.

2012-01-01

185

Resistance to cerebral malaria in tumor necrosis factor-alpha/beta-deficient mice is associated with a reduction of intercellular adhesion molecule-1 up-regulation and T helper type 1 response.  

PubMed Central

Tumor necrosis factor (TNF) induced by Plasmodium berghei ANKA (PbA) infection was suggested to play an important role in the development of cerebral malaria (CM). We asked whether TNF-alpha/beta double-deficient mice, which have a complete disruption of the TNF-signaling pathways, are protected from CM and what might be the possible mechanisms of protection. PbA infection induces fatal CM in wild-type mice, which die within 5 to 8 days with severe neurological signs. In contrast, TNF-alpha/beta-deficient mice are completely resistant to PbA-induced CM. As PbA-induced up-regulation of endothelial intercellular adhesion molecule (ICAM)-1 expression as well as the systemic release of nitric oxide is found only in wild-type mice, TNF is apparently central for the recruitment of mononuclear cells and microvascular damage. Mononuclear cell adhesion to the endothelium, vascular leak and, perivascular hemorrhage are found only in the brain of wild-type mice. By contrast, the development of parasitemia and anemia is independent of TNF. Resistance to CM in TNF-alpha/beta-deficient mice is associated with reduced interferon-gamma and interleukin-12 expression in the brain, in the absence of increased T helper type 2 cytokines. In conclusion, TNF apparently is required for PbA-induced endothelial ICAM-1 up-regulation and subsequent microvascular pathology resulting in fatal CM. In the absence of TNF, ICAM-1 and nitric oxide up-regulation are reduced, and PbA infection fails to cause fatal CM. Images Figure 3 Figure 4 Figure 5 Figure 6

Rudin, W.; Eugster, H. P.; Bordmann, G.; Bonato, J.; Muller, M.; Yamage, M.; Ryffel, B.

1997-01-01

186

Expression of Adhesion Molecules in Early Allergic Patch Test Reactions  

Microsoft Academic Search

In order to study the relevance of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1) and endothelial leukocyte adhesion molecule 1 (ELAM-1) for lymphocyte extravasation in the early phase of allergic contact dermatitis, the time courses of lymphocyte infiltration and adhesion molecule expression during initiation of this disorder were determined. Sequential biopsies of positive allergic patch test

J. Brasch; W. Sterry

1992-01-01

187

Shed soluble ICAM-1 molecules in bronchoalveolar lavage cell supernatants and serum of patients with pulmonary sarcoidosis  

Microsoft Academic Search

The soluble form of intercellular adhesion molecule-1 (sICAM-1) might be a serum parameter of inflammatory activity gauging\\u000a cellular interactions with possible relevance in sarcoidosis. To address this question we measured sICAM-1 by enzyme-linked\\u000a immunosorbent assay in serum and shedding of this molecule by bronchoalveolar lavage (BAL) cells in sarcoidosis patients (44\\u000a and 40, respectively) and in controls (10 and 19,

I. Bäumer; G. Zissel; M. Schlaak; J. Müller-Quernheim

1997-01-01

188

Monocyte Adhesion Molecules Expression in Patients with Chronic Hepatitis C Liver Disease  

PubMed Central

Background Chronic viral hepatitis is histologically characterized by predominantly periportal infiltration of mononuclear cells, including lymphocytes and monocytes/macrophages. Intralobular infiltration of these inflammatory cells is an ominous sign of deterioration and a criterion for disease activity. Objective To assess the monocyte inflammatory milieu, monocytes adhesion molecules, their endothelial receptors, cytokines and chemokines in patients with HCV induced chronic liver disease, in an attempt to clarify the role of blood monocytes in induction of inflammation and fibrogenesis in chronic hepatitis C liver disease. Subjects and Methods The current study included 60 patients with chronic liver disease categorized into 2groups: Patients chronic hepatitis C (CHC) and patients with liver cirrhosis (LC), 15 patients each; 15 healthy subjects were included as normal controls. Immunophenotype characterization was carried out by flowcytometric analysis for identification of CD11a, CD11b and CD49d monocyte surface antigen expression in different groups studied. The circulating levels of the soluble adhesion molecules (sE-selectin, sICAM-1 and sVCAM-1), cytokines (TNF-? and IL-1) and chemokines (MCP-1) were also assessed by immunoassays. Results Data demonstrated a significant increase (p<0.01) in the surface expression of CD11a on peripheral blood monocytes and in the circulating levels sE-selectins, sICAM-1, sVCAM-1 and TNF-? in both groups of patients compared to healthy subjects. Data also revealed a significant increase (p<0.01) in the surface expression of each of CD11b and CD49d on peripheral blood monocytes and in the circulating levels sICAM-1, sVCAM-1 and TNF-? in patients with LC compared to those with CHC. Moreover, data demonstrated that the increase in surface antigen expression of each CD11a (p<0.01), CD11b (p<0.05) and CD49d (p<0.01) on circulating peripheral blood monocytes is positively correlated with the increase in the circulating levels of each of sICAM-1 and sVCAM-1 in the both groups of patients. Conclusions These findings suggest that the modulation of monocyte-subset recruitment into the liver via adhesion molecules or cytokines/cytokine receptors may represent promising approaches for therapeutic interventions in human liver fibrosis. Measurement of serum soluble adhesion molecules may be useful for monitoring progression of liver inflammation and fibrosis during CHC.

El-Bassiouni, Nora E.I.; Mahmoud, Ola M.; El Ahwani, Eman G; Ibrahim, Raafat A.; El Bassiouny, Azza E.I.

2013-01-01

189

Platelet-derived growth factor BB mediates the glioma-induced migration of bone marrow-derived mesenchymal stem cells by promoting the expression of vascular cell adhesion molecule-1 through the PI3K, P38 MAPK and NF-?B pathways.  

PubMed

Platelet-derived growth factor BB (PDGFBB) has been shown to activate the migration of bone marrow-derived mesenchymal stem cells (BM-MSCs), and to contribute to mediating the tropism of BM-MSCs towards gliomas. However, the exact mechanism of this migratory behavior remains to be elucidated. The present study investigated the role of vascular cell adhesion molecule-1 (VCAM-1) in the PDGFBB-induced migration of BM-MSCs, the effect of PDGFBB on VCAM-1 expression of BM-MSCs and related signaling pathways involved in this process. Rat BM-MSCs were isolated and cultured by their characteristics of adherence to plastics. The concentrations of PDGFBB in the conditioned medium of C6 and U87 cells were measured using the ELISA method. In vitro migration assays using a VCAM-1 blocking antibody were performed to evaluate the role of VCAM-1 in PDGFBB-induced migration of BM-MSCs. The effect of rat recombinant PDGFBB on VCAM-1 expression of BM-MSCs was studied by RT-PCR and western blotting. LY294002, SB203580, PD98059, SP600125 and BAY11-7082 were used to explore the role of PI3K, p38 MAPK, MEK, JNK and NF-?B in the related intracellular signal transduction of PDGFBB stimulation on VCAM-1 expression of BM-MSCs. The data demonstrated that the neutralization of VCAM-1 inhibited the migration of BM-MSCs induced by PDGFBB. Additionally, PDGFBB stimulation increased VCAM-1 expression of BM-MSCs, which could be inhibited by LY294002, SB203580 and BAY11-7082. It is reasonable to conclude that PDGFBB significantly enhanced the expression of VCAM-1 in BM-MSCs, which facilitated the migration of BM-MSCs towards PDGFBB. PI3K, p38 MAPK and NF-?B were involved in the signal transduction of this process. PMID:24100802

Hu, Yi; Cheng, Peng; Ma, Jiang-Chun; Xue, Yi-Xue; Liu, Yun-Hui

2013-10-02

190

The influence of tobacco smoking on adhesion molecule profiles  

PubMed Central

Sequential interactions between several adhesion molecules and their ligands regulate lymphocyte circulation and leukocyte recruitment to inflammatory foci. Adhesion molecules are, therefore, central and critical components of the immune and inflammatory system. We review the evidence that tobacco smoking dysregulates specific components of the adhesion cascade, which may be a common factor in several smoking-induced diseases. Smoking causes inappropriate leukocyte activation, leukocyte-endothelial adhesion, and neutrophil entrapment in the microvasculature, which may help initiate local tissue destruction. Appropriate inflammatory reactions may thus be compromised. In addition to smoke-induced alterations to membrane bound endothelial and leukocyte adhesion molecule expression, which may help explain the above phenomena, smoking has a profound influence on circulating adhesion molecule profiles, most notably sICAM-1 and specific sCD44 variants. Elevated concentrations of soluble adhesion molecules may simply reflect ongoing inflammatory processes. However, increasing evidence suggests that specific soluble adhesion molecules are immunomodulatory, and that alterations to soluble adhesion molecule profiles may represent a significant risk factor for several diverse diseases. This evidence is discussed herein.

Scott, DA; Palmer, RM

2003-01-01

191

Plasma Soluble Adhesion Molecule Levels in Coronary Artery Ectasia  

Microsoft Academic Search

Background:Coronary artery ectasia (CAE) is defined as localized or diffuse dilatation of the coronary arteries. There are scarce data about the role of inflammation in CAE. In the present study, the plasma soluble adhesion molecules intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) levels in CAE were investigated. Methods: The study population (n = 67) consisted

Hale Yilmaz; Gulsah Tayyareci; Nurten Sayar; Ufuk Gurkan; Burak Tangurek; Recep Asilturk; Nihat Ozer; Sukru Aksoy; Dilek Simsek; Mehmet Yilmaz; Oner Engin; Aydin Cagil

2006-01-01

192

Wood adhesion and adhesives  

Treesearch

... to better understanding of the factors controlling the performance of the bonded ... other wood adhesives, especially when under the more severe durability tests. ... Keywords: Hot melt adhesives, pressure-sensitive adhesives, formaldehyde, ...

193

Indices of low-grade chronic inflammation in polycystic ovary syndrome and the beneficial effect of metformin  

Microsoft Academic Search

BACKGROUND: Women with polycystic ovary syndrome (PCOS) have an increased prevalence of insulin resistance (IR) and related disorders. Elevated serum levels of cellular adhesion molecules (CAMs) reflect low-grade chronic inflammation and have been associated with several insulin-resistant states. The objective of this study is to investigate whether soluble inflammatory markers (soluble intercellular adhesion molecule-1 (sICAM-1), soluble endothelial leu- kocyte adhesion

Evanthia Diamanti-Kandarakis; Thomas Paterakis; Krystallenia Alexandraki; Christina Piperi; Athanasios Aessopos; Ilias Katsikis; Nikolaos Katsilambros; George Kreatsas; Dimitrios Panidis

2006-01-01

194

Circulating Vascular Cell Adhesion Molecules VCAM-1, ICAM-1, and E-Selectin in Dependence on Aging  

Microsoft Academic Search

Background: Elevated levels of circulating cell adhesion molecules (cCAMs) such as vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and endothelial leukocyte adhesion molecule-1 (E-selectin) are found in subjects with vascular diseases and in subjects with several risk factors for atherosclerosis. However, data evaluating cCAMs and biological age are limited. Objective: The purpose of this study was to assess

Volker Richter; Fausi Rassoul; Kathrin Purschwitz; Bettina Hentschel; Wolfgang Reuter; Thomas Kuntze

2003-01-01

195

Long-distance running modulates the expression of leucocyte and endothelial adhesion molecules.  

PubMed

There still exist many unanswered questions whether physical exercise is beneficial or harmful to the immune system. The 'open-window' post-exercise hypothesis states that athletes are more susceptible to infections after exercise, but there is a need for further elucidation. The aim of the present study was to investigate the effect of long-distance running on leucocyte expression of selected adhesion molecules as well as the plasma levels of soluble leucocyte- and endothelium-derived adhesion molecules. Twenty-seven men participating in Oslo marathon together with 16 entrants (eight men and eight women) in the Oslo half-marathon were recruited to this study. Venous blood was collected before and immediately after the races for analysing the leucocyte expression of CD62L, CD11b and CD14 with the help of flow cytometry, and plasma concentrations of soluble (s) sE-selectin, sL-selectin, sP-selectin, sVCAM-1, sICAM-1 and sCD14 were assessed by means of enzyme-linked immunosorbent assays. A significant increase of leucocyte CD11b expression was observed following both races, compared to the pre-race situation. Monocyte CD14 expression increased only after the marathon race. After both races, CD62L expression was significantly lowered on all leucocyte subsets, whereas the plasma levels of sE-selectin, sP-selectin, sL-selectin, sVCAM-1, sICAM-1 and sCD14 were all increased. Altogether, these changes negatively influence the ability of leucocytes to adhere to and actively transmigrate the endothelium to reach the tissues. Our study thus supports the 'open-window' hypothesis, indicating a reduced capacity to combat infectious agents during the immediate post-exercise period. PMID:15379860

Nielsen, H G; Lyberg, T

2004-10-01

196

Early Upregulation of Endothelial Adhesion Molecules in Obese Hypertensive Men  

Microsoft Academic Search

Abstract—Upregulation of endothelial adhesion molecules is the earliest step of atherogenesis. Whether obesity induces endothelial adhesin upregulation is unknown. To address this topic, circulating vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), E-selectin, and von Willebrand factor (vWF) concentrations were evaluated in 22 obese hypertensive (51.464.6 years [mean6SD age]), 19 obese normotensive (50.663.8 years), 18 nonobese hypertensive (52.363.9 years),

Claudio Ferri; Giovambattista Desideri; Marco Valenti; Cesare Bellini; Mehtap Pasin; Anna Santucci; Giancarlo De Mattia

2010-01-01

197

Hypoxia Mediates Increased Neutrophil and Macrophage Adhesiveness to Alveolar Epithelial Cells  

Microsoft Academic Search

Leukocyte infiltration is known to play an important role in hypoxia-induced tissue damage. There is a paucity of informa- tion on the role of hypoxia in the expression of adhesion mol- ecules on respiratory epithelial cells. The current studies focus on the adhesion molecules intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), their expression pattern on alveolar epithelial

Beatrice Beck-Schimmer; Ralph C. Schimmer; Caveh Madjdpour; John M. Bonvini; Thomas Pasch; Peter A. Ward

2001-01-01

198

Priming of eosinophil adhesion in patients with birch pollen allergy during pollen season: Effect of immunotherapy  

Microsoft Academic Search

The adhesion of eosinophil granulocytes to E-selectin, vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) was investigated before and during birch pollen season in 24 patients allergic to birch pollen who had rhinoconjunctivitis and, in half of the cases, asthma during season. Half of the patients were undergoing specific immunotherapy for birch pollen allergy. Increased adhesion to VCAM-1

Lena Håkansson; Christina Heinrich; Sabina Rak; Per Venge

1997-01-01

199

Visual prognosis and vitreous molecules after vitrectomy for macular edema with branch retinal vein occlusion  

PubMed Central

This study investigated whether vascular endothelial growth factor (VEGF), soluble intercellular adhesion molecule-1 (sICAM-1), and pigment epithelium-derived factor (PEDF) influence the visual prognosis of patients with macular edema and branch retinal vein occlusion (BRVO). In 47 consecutive patients (47 eyes) undergoing vitrectomy, retinal thickness was examined by optical coherence tomography. Best-corrected visual acuity and the vitreous fluid levels of VEGF, sICAM-1, and PEDF were also determined. Patients were followed for at least 6 months after surgery. Vitreous fluid levels of VEGF and sICAM-1 were significantly lower in the patients with more marked improvement of visual acuity after vitrectomy, while PEDF was significantly higher. VEGF and sICAM-1 levels were significantly higher in patients with greater postoperative improvement of macular edema, while PEDF was significantly lower. In BRVO patients, vitreous fluid levels of VEGF, sICAM-1, and PEDF may influence both the response of macular edema to vitrectomy and the visual prognosis.

Noma, Hidetaka; Funatsu, Hideharu; Mimura, Tatsuya; Eguchi, Shuichiro; Shimada, Katsunori

2011-01-01

200

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

201

Puerarin Inhibits Adhesion Molecule Expression in TNF-?-Stimulated Human Endothelial Cells via Modulation of the Nuclear Factor ?B Pathway  

Microsoft Academic Search

Background: The isoflavone puerarin is the most abundant isoflavone-C-glucoside extracted from the root (radix puerariae) of the plant Pueraria lobata and possesses many biological activities. In this report, the ability of puerarin to modulate intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1) and endothelial leukocyte adhesion molecule 1 (E-selectin), and to induce changes in the nuclear factor

Wenzhi Hu; Qin Zhang; Xiangjun Yang; Yueying Wang; Lie Sun

2010-01-01

202

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

203

Opioid Control of Inflammatory Pain Regulated by Intercellular Adhesion Molecule1  

Microsoft Academic Search

Pain can be effectively controlled by endogenous mechanisms based on neuroimmune interactions. In inflamed tissue immune cell-derived opioid peptides activate opioid receptors on pe- ripheral sensory nerves leading to potent analgesia. This is brought about by a release of opioids from inflammatory cells after stimulation by stress or corticotropin-releasing hormone (CRH). Immunocytes migrate from the circulation to inflamed tissue in

Halina Machelska; Shaaban A. Mousa; Alexander Brack; Julia K. Schopohl; Heike L. Rittner; Michael Schafer; Christoph Stein

2002-01-01

204

Intercellular adhesion molecule-1 (ICAM-1) deficiency protects mice against severe forms of experimentally induced colitis  

PubMed Central

ICAM-1 (CD54), the ligand for LFA-1 and Mac-1, is up-regulated during inflammatory reaction on the activated vascular endothelium. To determine its role in intestinal inflammation, we induced acute experimental colitis in mice with a deleted ICAM-1 gene, by feeding them with 3% dextran sodium sulphate (DSS) in drinking water for 7 days. Chronic colitis was elicited by DSS similarly, followed by 2 weeks with water. In the acute phase of inflammation, ICAM-1-deficient mice exhibited a significantly lower mortality rate (5%) than control C57Bl/6J mice (35%). Control animals, but not the ICAM-1-deficient mice, exhibited diarrhoea and rectal bleeding. Histological examination of large-bowel samples evaluated the intensity of inflammatory changes, and type and extent of mucosal lesions. In the acute phase, 33.3% of samples from ICAM-1-deficient mice exhibited mucosal defects (flat and fissural ulcers), predominantly mild to moderate inflammatory infiltrate within the lamina propria mucosae and lower grades of mucosal lesions. Much stronger inflammatory changes were present in control animals, flat ulcers (sometimes multiple) and fissural ulcers being observed in 62.5% of samples. Mucosal inflammatory infiltrate was moderate to severe, typically with higher grades of mucosal lesions. In chronic colitis, smaller inflammatory changes were found in the large bowel. The two mouse strains differed, the chronic colitis being accompanied by an increased serum level of anti-epithelial IgA autoantibodies in C57Bl/6 control mice but not in ICAM-1-deficient mice. These findings provide direct evidence of the participation of ICAM-1 molecule in the development of experimentally induced intestinal inflammation.

Bendjelloul, F; Maly, P; Mandys, V; Jirkovska, M; Prokesova, L; Tuckova, L; Tlaskalova-Hogenova, H

2000-01-01

205

Lack of association between intercellular adhesion molecule-1 (ICAM-1) polymorphisms and polycystic ovary syndrome  

Microsoft Academic Search

Purpose  This study examined the possible association of G241R and K469E single nucleotide polymorphisms (SNPs) of ICAM-1 gene with the occurrence and clinical\\/biochemical characteristics of polycystic ovary syndrome (PCOS).\\u000a \\u000a \\u000a \\u000a \\u000a Methods  \\u000a G241R and K469E SNPs in DNA from peripheral blood leukocytes of 169 PCOS and 259 healthy control women were investigated by real-time PCR\\u000a combined with melting curve analysis using fluorescence-labeled hybridization

Pervin Vural; Müge Kanmaz-Özer; Semra Do?ru-Abbaso?lu; Ali Gedikba??; Esra Çil; Berrin Karada?; Müjdat Uysal

206

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

207

Mouse Cells Expressing Human Intercellular Adhesion Molecule1 Are Susceptible to Infection by Coxsackievirus A21  

Microsoft Academic Search

Competitive viral binding assays have revealed previously that coxsackievirus A21 (CAV21) and human rhinovirus14(HRV14)shareacommoncellsurfacereceptor.Morerecently,intercellularadhesionmolecule-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

DARREN R. SHAFREN; DOUGLAS J. DORAHY; SANDRA J. GREIVE; GORDON F. BURNS; ANDRICHARD D. BARRY

1997-01-01

208

Persistent Inflammation and Endothelial Activation in HIV-1 Infected Patients after 12 Years of Antiretroviral Therapy  

PubMed Central

Objective The study investigated markers of inflammation and endothelial activation in HIV infected patients after 12 years of successful combination antiretroviral treatment (cART). Methods Inflammation and endothelial activation were assessed by measuring levels of immunoglobulins, ?2-microglobulin, interleukin (IL) 8, tumor necrosis factor ? (TNF?), vascular cell adhesion molecule-1 (sVCAM-1), intercellular adhesion molecule-1 (sICAM-1), sE-Selectin, and sP-Selectin. Results HIV infected patients had higher levels of ?2-microglobulin, IL-8, TNF?, and sICAM-1 than uninfected controls, and HIV infected patients lacked correlation between platelet counts and sP-Selectin levels found in uninfected controls. Conclusion Discrete signs of systemic and vascular inflammation persist even after very long term cART.

Ronsholt, Frederikke F.; Ullum, Henrik; Katzenstein, Terese L.; Gerstoft, Jan; Ostrowski, Sisse R.

2013-01-01

209

Inhibition of ?-irradiation induced adhesion molecules and NO production by alginate in human endothelial cells  

Microsoft Academic Search

Inflammation is a frequent radiation-induced reaction following therapeutic irradiation. Treatment of human umbilical endothelial\\u000a cells (HUVEC) with ?-irradiation (?lR) induces the expression of adhesion proteins such as intercellular adhesion molecule-1\\u000a (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin. Since the upregulation of these proteins on endothelial\\u000a cell surface has been known to be associated with inflammation, interfering with the expression

Eun-Wha Son; Chul-Koo Cho; Dong-Kwon Rhee; Suhkneung Pyo

2001-01-01

210

Expression of cell adhesion molecules in primary renal disease and renal allograft rejection  

Microsoft Academic Search

IL-1: interleukin 1; MHC: major histocompatibility complex; PECAM-1: platelet endothelial cell adhesion Background. In vitro studies have demonstrated that inflammatory mediators such as the cytokines TNFa molecule-1; TNFa: tumour necrosis factor a; VCAM-1: vascular cell adhesion molecule-1. and IL-1 upregulate or induce de novo expression of cell adhesion molecules on endothelial and epithelial cells. In the present study the expression

I. A. Hauser; R. Riess; B. Hausknecht; H. Thuringer; R. B. Sterzel

1997-01-01

211

Intrauterine Adhesions  

MedlinePLUS

... uterus can occur. What are potential causes of Asherman syndrome? The most common cause of intrauterine adhesions is ... make periods lighter). What symptoms are associated with Asherman syndrome? A woman with intrauterine adhesions may have no ...

212

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

2013-01-28

213

Enhanced adhesion to laminin by apoptotic eosinophils.  

PubMed

Apoptotic cells are regarded as inert bodies that turn off intracellular processes and functional capabilities. The objective was to study adhesion by eosinophils in relation to the apoptotic process. Eosinophils were cultured for up to 72 h. The living cells were separated from the apoptotic cells, and their adhesion to transfected cell lines expressing vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), E-selectin and laminin was measured. To relate the functional studies with cell structure, the surface receptor expression of beta1- and beta2-integrins was investigated by flow cytometry. Apoptotic eosinophils evidenced an increased expression of the alpha-chain of the laminin receptor and CD49f and an increased ability to adhere to a laminin-coated surface. Adhesion to the endothelial cell adhesion receptors E-selectin, VCAM-1 and ICAM-1 was absent in apoptotic eosinophils and was paralleled by a low expression of CD11b, CD29, CD49d and CD66b. The specifically increased adhesion to laminin and expression of the laminin receptor alpha-chain is a unique feature of apoptotic eosinophils. When an eosinophil goes into apoptosis, it still possesses the ability to interact with its environment. Our results point to new ideas as to how the apoptotic eosinophil behaves in apoptosis. PMID:14507306

Seton, K; Håkansson, L; Venge, P

2003-10-01

214

Circulating cell adhesion molecules and endothelial markers before and after transluminal angioplasty in peripheral arterial occlusive disease  

Microsoft Academic Search

In the present study, the levels of soluble adhesion molecules P- and E-selectin, intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1) and of other markers of endothelial activation or injury, such as thrombomodulin, von Willebrand factor (vWF), as well as homocysteine, were prospectively investigated in 71 patients (21 women, 50 men, age 68±13) with predominantly femoropopliteal peripheral arterial occlusive disease

Dimitrios A. Tsakiris; Martin Tschöpl; Kurt Jäger; Walter E. Haefeli; Francine Wolf; German A. Marbet

1999-01-01

215

Soluble ICAM-1 serum levels in patients with intermediate uveitis  

PubMed Central

AIM—To investigate whether serum levels of soluble intercellular adhesion molecule 1 (sICAM-1) can serve as a marker of the presence of systemic disease in intermediate uveitis.?METHODS—In a multicentre study sICAM-1 serum levels were measured in 61 patients with idiopathic intermediate uveitis, controls included 56 uveitis patients with a systemic disease (26 sarcoid associated uveitis and 30 HLA-B27 positive acute anterior uveitis), 58 uveitis patients without systemic disease (30 toxoplasma chorioretinitis and 28 Fuchs' hetrochromic cyclitis), and 21 normal controls. The clinical records of the patients with intermediate uveitis were analysed for disease characteristics at the time of blood sampling and for a relation with the development of a systemic disease after a mean follow up of 4.5 years. ?RESULTS—Increased serum levels of sICAM-1 were found in 34 out of 61 patients with intermediate uveitis and were significantly different when compared with toxoplasmosis, Fuchs' cyclitis, and healthy controls (p<0.001). Elevated sICAM-1 levels were also found in 18 out of 26 patients with sarcoid uveitis and in 11 out of 30 patients with HLA-B27 associated anterior uveitis. Raised sICAM-1 levels in the intermediate uveitis group were significantly associated with active ocular disease (p<0.01) and the presence of vitreous exudates (p<0.05). Increased levels of sICAM-1 correlated with interleukin 8 levels (IL-8) (tested in a previous study in the same group of intermediate uveitis patients) in patients with active systemic involvement. Follow up of the patients showed that an established or suspected systemic disease was found more often in the 21 intermediate uveitis patients with increased sICAM-1 and IL-8 levels compared with the other 40 patients with intermediate uveitis (p<0.01).?CONCLUSIONS—The measurement of both sICAM-1 and IL-8 can be used as a marker for ocular disease activity and for a predisposition of developing an associated systemic disease in intermediate uveitis patients.??

Klok, A.; Luyendijk, L.; Zaal, M.; Rothova, A.; Kijlstra, A.

1999-01-01

216

The impact of serum lipid levels on circulating soluble adhesion molecules in childhood.  

PubMed

Cell adhesion molecules play a rather important role in the development of atherosclerosis mediating the attachment of monocytes to the endothelium. It has also been well established that hyperlipidemia is a risk factor for atherosclerosis from childhood. The aim of this study was to investigate whether the soluble adhesion molecules correlate with the circulating lipid levels in children. The study population consisted of 107 children (64 boys, 43 girls) aged 6-13 y. Parental history of cardiovascular disease, age, gender, and anthropometric parameters were recorded in all children. Blood samples were obtained from every child following a 12-hour fasting period. Serum triglycerides, total cholesterol, and its fractions as well as plasma levels of P and E selectins and adhesion molecules sVCAM-1 and sICAM-1 were determined. After controlling for age and body mass index, both sVCAM-1 and sP-selectin levels were inversely associated with HDL values (r = -0.33, p = 0.005 and r = -0.39, p = 0.001, respectively). A significant positive correlation was found between sVCAM-1 and triglycerides (r = 0.48, p < 0.001). An increment of 10 mg/dL of HDL corresponds to about 50% reduction of the odds for endothelial dysfunction whereas an increment of 10 mg/dL of triglyceride levels indicates a more than 3-fold excess risk, using either sP-selectin or sVCAM-1 levels as a surrogate for the determination of endothelial dysfunction. We suggest that HDL-C and triglycerides correlate in a biologically plausible way with soluble adhesion molecules, which therefore could be considered as useful indicators of the process of preclinical atherosclerosis even from childhood. PMID:12193684

Kavazarakis, Emmanuel; Moustaki, Maria; Gourgiotis, Dimitros; Zeis, Petros M; Bossios, Apostolos; Mavri, Antonia; Chronopoulou, Agelliki; Karpathios, Themistocles

2002-09-01

217

In situ Expression of Cytokines and Cellular Adhesion Molecules in the Skin of Patients with Systemic Sclerosis  

Microsoft Academic Search

Cytokines and cellular adhesion molecules (CAMs) may play a role in the inflammatory and fibrotic processes underlying systemic sclerosis (SSc). We compared the immunohistological distribution of cytokines and CAMs in skin biopsies from 12 SSc patients and 14 normal (NL) individuals. Among CAMs, vascular cell adhesion molecule-1 (VCAM-1), which mediates leukocyte-endothelial adhesion, showed increased expression on SSc versus NL endothelium

Alisa E. Koch; Lisa B. Kronfeld-Harrington; Zoltan Szekanecz; Michael M. Cho; Kenneth Haines; Lisa A. Harlow; Robert M. Strieter; Steven L. Kunkel; Mary C. Massa; Walter G. Barr; Sergio A. Jimenez

1993-01-01

218

Adhesive capsulitis.  

PubMed

Adhesive capsulitis is a common problem seen in the general population by orthopedic surgeons. It is a problem that causes patients pain and disability, and symptoms can last up to 2 years and longer. The questions of when and how to treat the frozen shoulder can present challenges. Most treatments are conservative; however, indications for surgery do exist. Arthroscopic capsular release has gained popularity over the years and offers a predictably good treatment in patients with adhesive capsulitis. The purpose of this paper is to review the orthopedic literature on adhesive capsulitis, to provide background information on this topic, and to describe our technique in arthroscopic capsular release. PMID:18004221

Tasto, James P; Elias, David W

2007-12-01

219

Adhesion molecules  

Microsoft Academic Search

Adhesion molecules are cell membrane receptors that mediate cell-to-cell and cell-to-matrix communication in macroorganisms. Because the receptors and ligands involved are non-diffusible, adhesion molecules are capable of organ, tissue and cell specific regulation under physiological and pathophysiological conditions. Consequently, this local (positional) regulatory system has the ability to alter\\/modify\\/tune systemic regulatory signals and generate signals locally in order to match

Istvan Berczi; Andor Szentivanyi

2003-01-01

220

Effect of cysteine protease of Porphyromonas gingivalis on adhesion molecules in gingival epithelial cells.  

PubMed

We examined the effect of cysteine protease of Porphyromonas gingivalis (P. gingivalis) on cell adhesion molecules including intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and very late antigen-4 (VLA-4) of human gingival epithelial cells. The cells were incubated for 48 hr with or without P. gingivalis protease. Their cell adhesion molecule expression levels were increased at 12 hr, but decreased at 18-48 hr. This result suggests that protease degrades cell adhesion molecules. After the stimulation with protease for 12 hr, P. gingivalis fimbrial binding to a monolayer of the cells was effectively inhibited by the addition of the cell adhesion molecules, suggesting the fimbrial binding to the cells occurred through cell surface adhesion molecules. PMID:10446759

Wang, P L; Shinohara, M; Murakawa, N; Endo, M; Sakata, S; Okamura, M; Ohura, K

1999-05-01

221

Tumor Necrosis factor-alpha Induces Adhesion Molecule Expression through the Sphingosine Kinase Pathway  

Microsoft Academic Search

The signaling pathways that couple tumor necrosis factor-alpha (TNFalpha ) receptors to functional, especially inflammatory, responses have remained elusive. We report here that TNFalpha induces endothelial cell activation, as measured by the expression of adhesion protein E-selectin and vascular adhesion molecule-1, through the sphingosine kinase (SKase) signaling pathway. Treatment of human umbilical vein endothelial cells with TNFalpha resulted in a

Pu Xia; Jennifer R. Gamble; Kerry-Anne Rye; Lijun Wang; Charles S. T. Hii; Peter Cockerill; Yeesim Khew-Goodall; Andrew G. Bert; Philip J. Barter; Mathew A. Vadas

1998-01-01

222

Expression of the kidney injury molecule 1 in the rat cochlea and induction by cisplatin  

Microsoft Academic Search

Cisplatin is a widely used chemotherapeutic agent whose dose-limiting side effects include ototoxicity and nephrotoxicity. Recent evidence indicates that cisplatin induces the expression of a novel protein, kidney injury molecule-1, in the renal proximal tubular epithelium to aid in regeneration. In this study, we determined whether kidney injury molecule-1 is expressed in the cochlea and is induced by cisplatin. Using

D. Mukherjea; C. A. Whitworth; S. Nandish; G. A. Dunaway; L. P. Rybak; V. Ramkumar

2006-01-01

223

Differential adhesion pattern of B cell chronic lymphocytic leukemia cells.  

PubMed

Binding of B cell chronic lymphocytic leukemia (B-CLL) cells to other cells and to extracellular matrices influences the pathophysiology and the clinical presentation of the B-CLL disease. It is still unknown which adhesion pathways regulate the traffic of B-CLL cells within distinct histologic compartments of lymphoid organs. In addition, it is not yet clarified which mechanisms mediate the intercellular adhesion of B-CLL cells. The present study sought to identify the mechanisms that are involved in the binding of B-CLL cells to secondary lymphoid organs in situ and in the homotypic aggregation of these cells. B-CLL cells specifically bound to germinal centers of normal human tonsils via the adhesion pair integrin alpha4beta1/vascular cell adhesion molecule-1 (VCAM-1). Among a large panel of antibodies tested only mAbs against CD19 induced homotypic adhesion of B-CLL cells via the adhesion molecules integrin alphaL (leukocyte function antigen-1 (LFA-1)), intercellular adhesion molecule-1 (ICAM-1) and CD21. Anti-CD19-induced aggregation required protein synthesis. We hypothesize that the observed heterotypic and homotypic adhesion of B-CLL cells reflects the ability of these leukemic cells to migrate in vivo. PMID:9436923

Behr, S I; Korinth, D; Schriever, F

1998-01-01

224

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

225

Endothelial Cell E- and P-Selectin and Vascular Cell Adhesion Molecule1 Function as Signaling Receptors  

Microsoft Academic Search

Previous studies have shown that polymor- phonuclear leukocyte (PMN) adherence to endothelial cells (EC) induces transient increases in EC cytosolic free calcium concentration ((Ca 2 1 ) i ) that are required for

P. Lorenzon; E. Vecile; E. Nardon; E. Ferrero; J. M. Harlan; F. Tedesco; A. Dobrina

1998-01-01

226

Small low-density lipoproteins and vascular cell adhesion molecule-1 are increased in association with hyperlipidemia in preeclampsia  

Microsoft Academic Search

The pregnancy disorder preeclampsa is characterized by endothelial cell dysfunction that may be promoted by abnormal increases in circulating lipids, particularly triglycerides and free fatty acids. Serum triglyceride concentration is a major regulatory determinant of low-density lipoprotein (LDL) size and density distribution. Smaller, denser LDL particles have several intrinsic properties capable of inducing endothelial dysfunction. The present nested, case-control study

Carl A. Hubel; Fiona Lyall; Lisa Weissfeld; Robin E. Gandley; James M. Roberts

1998-01-01

227

Adhesive plasters  

DOEpatents

Adhesive plaster compositions are provided by treating particles of Y.sub.2 O.sub.3, Eu.sub.2 O.sub.3, Gd.sub.2 O.sub.3 or Nd.sub.2 O.sub.3 with dilute acid solutions. The resulting compositions have been found to spontaneously harden into rigid reticulated masses resembling plaster of Paris. Upon heating, the hardened material is decomposed into the oxide, yet retains the reticulated rigid structure.

Holcombe, Jr., Cressie E. (Knoxville, TN); Swain, Ronald L. (Concord, TN); Banker, John G. (Kingston, TN); Edwards, Charlene C. (Knoxville, TN)

1978-01-01

228

Intrauterine adhesions.  

PubMed

Joseph Asherman first described intrauterine adhesions in 1948. It is commonly referred to as Asherman's syndrome and intrauterine synechiae. It is characterized by a spectrum ranging from amenorrhea to menstrual disturbance to normal menses. It is frequently associated with infertility. The true incidence is unknown. Most cases occur within close temporal proximity to a pregnancy, usually within 4 months and usually while the woman is in a hypoestrogenized state. Most cases are associated with trauma to the endometrium from surgical procedures, primarily curettage. Increasingly, cases are associated with myomectomy both abdominal and hysteroscopic, removal of septae, and any other intrauterine surgery. Pathology shows fibrous connective tissue bands with or without glandular tissue, although this may range from filmy to dense. The diagnosis is primarily by history and a high index of suspicion. Confirmatory tests are increasingly saline infusion hysterography (SIS) or hysterosalpingogram (HSG), although magnetic resonance imaging has also been used. Ultimately, hysteroscopy is employed for the final diagnosis and treatment. Hysteroscopic lysis of adhesions is the main method of treatment. Dense scar tissue and difficult entry into the cervix may require laparoscopic or ultrasound guidance. Most authors use an intrauterine stent and follow treatment with sequential estrogen and progesterone therapy. Increasingly early intervention either with repeat SIS or HSG or most recently with flexible hysteroscopy has been advocated. Treatments outcomes are difficult to assess as there are no universally agreed upon classification system. However, intrauterine pregnancies rates range from 22 to 45% and live births range from 28 to 32%. The risk of complications for those that achieve pregnancy is significant with a significant risk for placenta accreta and subsequent blood loss, transfusion, and hysterectomy. Prospective controlled studies are needed to determine the best diagnostic and treatments for intrauterine adhesions. PMID:18756412

Berman, Jay M

2008-07-01

229

Dental Adhesives: A Perspective.  

National Technical Information Service (NTIS)

A study based on the laboratory characterization of four adhesive restoratives was conducted. The findings indicated that adhesion of three of the materials to the components of tooth structure was unreliable. Strength properties of adhesive systems of th...

E. F. Huget S. G. Vermilyea J. M. Vilca

1978-01-01

230

Handbook of Soviet Adhesives.  

National Technical Information Service (NTIS)

The report presents a narrative analysis of Soviet conventional and high-performance adhesive and tabular data on the properties, compositions, designations, and characteristics of the adhesive material. It presents potential or known uses of the adhesive...

H. Jaffe G. G. Orpanides A. F. Readdy

1974-01-01

231

Interleukin 18 and sICAM-1 serum levels in families with type 1 diabetes mellitus  

Microsoft Academic Search

It is well known that subjects with type 1 diabetes are at an increased risk of death from coronary heart disease in comparison to non-diabetic age-matched individuals because hyperglycaemia is believed to be a key risk factor for the development of micro- and macrovascular complica- tions. On the other hand there is increasing evidence about the role of inflammatory mediators

Wawrusiewicz-Kurylonek N; Kinalska I

2005-01-01

232

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

233

Adhesion to Sintered Substrates  

Microsoft Academic Search

Although the consensus is that various forms of specific adhesion are prevalent in most adhesive systems, the importance of mechanical adhesion should not be overlooked. Cylindrical substrates of stainless steel, both the dense metal and in sintered form, have been bonded with a polyurethane “adhesive” and subjected to torsional shear loading. Overall strain and load at failure are considerably higher

Martin E. R. Shanahan; Alun E. P. Morris

1996-01-01

234

Adhesion molecules in pediatric intensive care patients with organ dysfunction syndrome  

Microsoft Academic Search

Objective  To determine serum concentrations of the soluble forms of vascular cell adhesion molecule 1 (VCAM-1), intracellular adhesion\\u000a molecule 1 (ICAM-1), and E-selectin in ventilated neonatal and pediatric intensive care patients with varying severity of\\u000a multiorgan dysfunction syndrome (MODS) with or without infection-triggered organ failure.\\u000a \\u000a \\u000a \\u000a Design and setting  Prospective pilot study, a level III neonatal and pediatric intensive care unit at a University children's

Marcus Krueger; Andrea Heinzmann; Markus Nauck

2007-01-01

235

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

236

Variant antigens and endothelial receptor adhesion in Plasmodium falciparum.  

PubMed

Parasite-derived proteins expressed on the surface of erythrocytes infected with Plasmodium falciparum are important virulence factors, since they mediate binding of infected cells to diverse receptors on vascular endothelium and are targets of a protective immune response. They are difficult to study because they undergo rapid clonal antigenic variation in vitro, which precludes the derivation of phenotypically homogeneous cultures. Here we have utilized sequence-specific proteases to dissect the role of defined antigenic variants in binding to particular receptors. By selection of protease-resistant subpopulations of parasites on defined receptors we (i) confirm the high rate of antigenic variation in vitro; (ii) demonstrate that a single infected erythrocyte can bind to intercellular adhesion molecule 1, CD36, and thrombospondin; (iii) show that binding to intercellular adhesion molecule 1 and CD36 are functions of the variant antigen; and (iv) suggest that binding to thrombospondin may be mediated by other components of the infected erythrocyte surface. PMID:8622966

Gardner, J P; Pinches, R A; Roberts, D J; Newbold, C I

1996-04-16

237

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

238

Activation of LFA-1 through a Ca2+-dependent Epitope Stimulates Lymphocyte Adhesion  

Microsoft Academic Search

The leukocyte function-associated molecule-1 (LFA-1) plays a key role in cell adhesion processes between cells of the immune system. We in- vestigated the mechanism that may regulate LFA- 1-1igand interactions, which result in cell-cell adhe- sion. To this end we employed an intriguing anti-LFA-1 ot mAb (NKI-L16), capable of inducing rather than inhibiting cell adhesion. Aggregation induced by NKI- L16

Yvette van Kooyk; Pauline Weder; Frans Hogervorst; Arthur J. Verhoeven; Gijs van Seventer

239

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

240

Relationships of Circulating Carotenoid Concentrations with Several Markers of Inflammation, Oxidative Stress, and Endothelial Dysfunction: The Coronary Artery Risk Development in Young Adults (CARDIA)/Young Adult Longitudinal Trends in Antioxidants (YALTA) Study  

PubMed Central

Background Serum carotenoid concentrations relate inversely to cardiovascular disease incidence. To clarify the effect of carotenoids on atherosclerotic risk factors, we examined the association of circulating carotenoids with inflammation, oxidative stress, endothelial dysfunction, and smoking. Methods Black and white men and women in the Coronary Artery Risk Development in Young Adults study, ages 18 to 30 years at recruitment (1985–1986) from 4 US cities, were investigated over 15 years. We included 2048 to 4580 participants in analyses of the sum of serum ?-carotene, ?-carotene, zeaxanthin/lutein, and ?-cryptoxanthin concentrations and of lycopene at year 0 and at year 7. Results The year 0 sum of 4 carotenoids was inversely associated (all P <0.05) with year 0 leukocyte count (slope per sum carotenoid SD, ?0.17); year 7 fibrinogen (slope, ?0.10); year 7 and year 15 C-reactive protein (slope, ?0.12 and ?0.09); and year 15 F2-isoprostanes (slope, ?13.0), soluble P-selectin (slope, ?0.48), and soluble intercellular adhesion molecule-1 (sICAM1; slope, ?5.1). Leukocyte counts and sICAM1 and F2-isoprostane concentrations had stronger associations in smokers than in nonsmokers, and sICAM1 concentrations were higher in the highest carotenoid quartile in smokers than in the lowest carotenoid quartile in nonsmokers. Superoxide dismutase was positively associated with the sum of 4 carotenoids (slope, 0.12; P <0.01). Lycopene was inversely associated only with sICAM1. The year 7 carotenoid associations with these markers were mostly similar to those at year 0. Conclusions Circulating serum carotenoids were associated, some interactively with smoking, in apparently beneficial directions with markers of inflammation, oxidative stress, and endothelial dysfunction.

Hozawa, Atsushi; Jacobs, David R.; Steffes, Michael W.; Gross, Myron D.; Steffen, Lyn M.; Lee, Duk-Hee

2008-01-01

241

Oral green tea catechins transiently lower plasma glucose concentrations in female db/db mice.  

PubMed

Polyphenols, including green tea catechins, are secondary plant compounds often discussed in the context of health-promoting potential. Evidence for such effects is mainly derived from epidemiological and cell culture studies. The aim of the present study was to investigate antidiabetic, antiadipogenic, and anti-inflammatory effects at nonpharmacological doses in an obese diabetic mouse model that exerts early relevant clinical signs of non-insulin-dependent diabetes mellitus. Female db/db mice received a flavonoid-poor diet either without additive, with rosiglitazone (RSG, 0.02 g/kg diet), or with green tea extract (low-dose green tea extract [LGTE] and high-dose green tea extract [HGTE], 0.1 and 1 g/kg diet). Food and water were freely available. The body weight was monitored weekly. Blood was sampled (12-h fasted) from the tail vein on day 28 and analyzed for glucose, cholesterol, triacylglycerol, nonesterified fatty acids, insulin, adiponectin, and soluble intercellular adhesion molecule-1 (sICAM-1). Blood glucose was also analyzed on day 14. Furthermore, sICAM-1 release was investigated in tumor necrosis factor alpha-stimulated EAhy926 cells. After 14 days, fasting glycemia was improved by RSG or HGTE supplementation compared to controls. However, at the end of the study (day 28), only RSG exhibited glucose-lowering effects and induced plasma adiponectin concentrations, paralleled by higher body weight gain and reduced periuterine fat pads compared to controls. However, only GTE treatment reduced sICAM-1 release in vitro and in vivo. Nonpharmacological HGTE supplementation in db/db mice caused (1) no adiponectin-inducing or antiadipogenic effects, (2) reduced sICAM-1 release, thereby potentially exerting anti-inflammatory effects in the progressive diabetic state, and (3) a transient improvement in glycemia. PMID:23514230

Wein, Silvia; Schrader, Eva; Rimbach, Gerald; Wolffram, Siegfried

2013-03-20

242

Cell adhesion in cancer  

Microsoft Academic Search

Cell adhesion is a key physiological event tightly coupled to other major cellular processes coordinating morphogenesis and histogenesis. Cell-to-cell and cell-to-extracellular matrix adhesion regulates the social behavior of cells in developing embryos and in the adult. These two adhesion systems also play a critical role in pathogenesis. In vertebrates, more than 3% of genes are thought to encode adhesion molecules.

Jean Paul Thiery

2003-01-01

243

Denture adhesive articles  

US Patent & Trademark Office Database

The present invention relates to a denture adhesive article comprising: a) a safe and effective adhesive amount of a water soluble denture adhesive component; b) a safe and effective amount of a component selected from the group consisting of a water soluble plasticizer, a water soluble carrier, and mixtures thereof; wherein the article is bioerodible; and wherein the article has dry tack.

Rajaiah; Jayanth (Loveland, OH); Wilder; Elizabeth Anne (West Chester, OH); Hamersky; Mark William (Fairfield Township, OH); Smith; Steven Daryl (Fairfield, OH); Scott; Douglas Craig (Loveland, OH)

2010-11-16

244

Medical polymer adhesives  

Microsoft Academic Search

A critical survey of literature data on medical polymer adhesives is presented Various classes of polymers are discussed from the point of view of their application in surgery.\\u000a Cyanacrylate adhesives are described along with some data on the strength of adhesive joints of living tissues, the processes of biodegradation and elimination from the organism, and the reaction of living tissues

T. E. Lipatova; Ukrainian SSR

245

Mini-review: barnacle adhesives and adhesion.  

PubMed

Barnacles are intriguing, not only with respect to their importance as fouling organisms, but also in terms of the mechanism of underwater adhesion, which provides a platform for biomimetic and bioinspired research. These aspects have prompted questions regarding how adult barnacles attach to surfaces under water. The multidisciplinary and interdisciplinary nature of the studies makes an overview covering all aspects challenging. This mini-review, therefore, attempts to bring together aspects of the adhesion of adult barnacles by looking at the achievements of research focused on both fouling and adhesion. Biological and biochemical studies, which have been motivated mainly by understanding the nature of the adhesion, indicate that the molecular characteristics of barnacle adhesive are unique. However, it is apparent from recent advances in molecular techniques that much remains undiscovered regarding the complex event of underwater attachment. Barnacles attached to silicone-based elastomeric coatings have been studied widely, particularly with respect to fouling-release technology. The fact that barnacles fail to attach tenaciously to silicone coatings, combined with the fact that the mode of attachment to these substrata is different to that for most other materials, indicates that knowledge about the natural mechanism of barnacle attachment is still incomplete. Further research on barnacles will enable a more comprehensive understanding of both the process of attachment and the adhesives used. Results from such studies will have a strong impact on technology aimed at fouling prevention as well as adhesion science and engineering. PMID:23802872

Kamino, Kei

2013-01-01

246

A new class of obesity genes encodes leukocyte adhesion receptors.  

PubMed

Obesity is a complex disease, and multiple genes contribute to the trait. The description of five genes (ob, db, tub, Ay, and fat) responsible for distinct syndromes of spontaneous monogenic obesity in mice has advanced our knowledge of the genetics of obesity. However, many other genes involved in the expression of this disease remain to be determined. We report here the identification of an additional class of genes involved in the regulation of adipose tissue mass. These genes encode receptors mediating leukocyte adhesion. Mice deficient in intercellular adhesion molecule-1 became spontaneously obese in old age on normal mouse chow or at a young age when provided with a diet rich in fat. Mice deficient in the counterreceptor for intercellular adhesion molecule-1, the leukocyte integrin alphaMbeta2 (Mac-1), showed a similar obesity phenotype. Since all mice consumed approximately the same amount of food as controls, the leukocyte function appears to be in regulating lipid metabolism and/or energy expenditure. Our results indicate that (i) leukocytes play a role in preventing excess body fat deposition and (ii) defects in leukocyte adhesion receptors can result in obesity. PMID:9207125

Dong, Z M; Gutierrez-Ramos, J C; Coxon, A; Mayadas, T N; Wagner, D D

1997-07-01

247

TNF-? Antagonism with Etanercept Decreases Glucose and Increases the Proportion of High Molecular Weight Adiponectin in Obese Subjects with Features of the Metabolic Syndrome  

PubMed Central

Context and Objective: Obesity is associated with activation of the TNF-? system, increased inflammatory markers, and insulin resistance. Although studies in rodents suggest that attenuation of TNF activity improves glucose homeostasis, the effect of prolonged inhibition of TNF-? with etanercept on inflammation and glucose homeostasis in a human model of obesity is not known. Design and Participants: Forty obese subjects with features of metabolic syndrome were randomized to etanercept or placebo, 50 mg twice weekly for 3 months, followed by 50 mg once weekly for 3 months. Outcome Measures: Subjects underwent oral glucose tolerance testing and measurement of serum inflammatory biomarkers and adipokines. Subcutaneous fat biopsy was performed in a subset for measurement of adipokine and TNF-? mRNA expression. Results: Visceral adiposity was significantly associated with serum concentrations of TNF receptor 1 (TNFR1), TNFR2, and vascular cell adhesion molecule-1 and adipose tissue expression of TNF-? and SOCS-3 (all P < 0.05). Insulin resistance as assessed by homeostasis model assessment was significantly associated with TNFR1, C-reactive protein, IL-6, and soluble intracellular adhesion molecule-1 (sICAM-1) (all P < 0.05). Etanercept significantly improved fasting glucose (treatment effect vs. placebo over 6 months, ?10.8 ± 4.4%, P = 0.02). Etanercept also increased the ratio of high molecular weight adiponectin to total adiponectin (+22.1 ± 9.2% vs. placebo, P = 0.02), and decreased levels of sICAM-1 (?11 ± 2% vs. placebo, P < 0.0001). In contrast, body composition, lipids, C-reactive protein, and IL-6 were unchanged after 6 months. Conclusions: Prolonged therapy with etanercept improved fasting glucose, increased the ratio of high molecular weight to total adiponectin, and decreased sICAM-1 in obese subjects with abnormal glucose homeostasis and significant subclinical inflammation.

Stanley, Takara L.; Zanni, Markella V.; Johnsen, Stine; Rasheed, Sarah; Makimura, Hideo; Lee, Hang; Khor, Victor K.; Ahima, Rexford S.; Grinspoon, Steven K.

2011-01-01

248

Structural equation modeling of the inflammatory response to traffic air pollution.  

PubMed

Several epidemiological studies have reported conflicting results on the effect of traffic-related pollutants on markers of inflammation. In a Bayesian framework, we examined the effect of traffic pollution on inflammation using structural equation models (SEMs). We studied measurements of C-reactive protein (CRP), soluble vascular cell adhesion molecule-1 (sVCAM-1), and soluble intracellular adhesion molecule-1 (sICAM-1) for 749 elderly men from the Normative Aging Study. Using repeated measures SEMs, we fit a latent variable for traffic pollution that is reflected by levels of black carbon, carbon monoxide, nitrogen monoxide and nitrogen dioxide to estimate its effect on a latent variable for inflammation that included sICAM-1, sVCAM-1 and CRP. Exposure periods were assessed using 1-, 2-, 3-, 7-, 14- and 30-day moving averages previsit. We compared our findings using SEMs with those obtained using linear mixed models. Traffic pollution was related to increased inflammation for 3-, 7-, 14- and 30-day exposure periods. An inter-quartile range increase in traffic pollution was associated with a 2.3% (95% posterior interval (PI): 0.0-4.7%) increase in inflammation for the 3-day moving average, with the most significant association observed for the 30-day moving average (23.9%; 95% PI: 13.9-36.7%). Traffic pollution adversely impacts inflammation in the elderly. SEMs in a Bayesian framework can comprehensively incorporate multiple pollutants and health outcomes simultaneously in air pollution-cardiovascular epidemiological studies. PMID:23232970

Baja, Emmanuel S; Schwartz, Joel D; Coull, Brent A; Wellenuis, Gregory A; Vokonas, Pantel S; Suh, Helen H

2012-12-12

249

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

250

Regulation of Interleukin-5-Induced ?2-Integrin Adhesion of Human Eosinophils by Phosphoinositide 3-Kinase  

PubMed Central

We examined the role of phosphoinositide 3-kinase (PI3K) in integrin-mediated eosinophil adhesion. ?p85, a dominant-negative form of the class IA PI3K adaptor subunit, was fused to an HIV-TAT protein transduction domain (TAT-?p85). Recombinant TAT-?p85 inhibited interleukin (IL)-5–stimulated phosphorylation of protein kinase B, a downstream target of PI3K. ?2-Integrin–dependent adhesion caused by IL-5 to the plated intracellular adhesion molecule-1 surrogate, bovine serum albumin, was inhibited by TAT-?p85 in a concentration-dependent manner. Similarly, two PI3K inhibitors, wortmannin and LY294002, blocked eosinophil adhesion to plated bovine serum albumin. By contrast, ?1-integrin–mediated eosinophil adhesion to vascular cell adhesion moelcule-1 was not blocked by TAT-?p85, wortmannin, or LY294002. Rottlerin, a protein kinase C (PKC)-? inhibitor, also blocked ?2-integrin adhesion of eosinophils caused by IL-5, whereas ?1 adhesion to vascular cell adhesion molecule-1 was not affected. IL-5 caused translocation of PKC? from the cytosol to cell membrane; inhibition of PI3K by wortmannin blocked translocation of PKC?. Western blot analysis demonstrated that extracellular signal–regulated kinase phosphorylation, a critical intermediary in adhesion elicited by IL-5, was blocked by inhibition of either PI3K or PKC-?. These data suggest that extracellular signal–regulated kinase–mediated adhesion of ?2-integrin caused by IL-5 is mediated in human eosinophils by a class IA PI3K through activation of a PKC? pathway.

Sano, Masaaki; Leff, Alan R.; Myou, Shigeharu; Boetticher, Evan; Meliton, Angelo Y.; Learoyd, Jonathan; Lambertino, Anissa T.; Munoz, Nilda M.; Zhu, Xiangdong

2005-01-01

251

Nuclear factor kappaB-mediated down-regulation of adhesion molecules: possible mechanism for inhibitory activity of bigelovin against inflammatory monocytes adhesion to endothelial cells.  

PubMed

The flowers of Inula britannica L. var. chinensis (Rupr.) Reg. (Compositae) are used in traditional medicine to treat asthma, chronic bronchitis, and acute pleurisy in China and Korea. However, the pharmacological actions of Inula britannica L. var. chinensis on endothelial cells and inflammatory monocytes are not clear. In this study, we investigated whether bigelovin, a sesquiterpene lactone isolated from the flowers of Inula britannica L. var. chinensis, inhibits monocyte adhesion and adhesion molecule expression in brain endothelial cells. We measured tumor necrosis factor-alpha (TNF-alpha)-enhanced Raw264.7 monocyte binding to brain endothelial cells and the levels of cell adhesion molecules, including vascular adhesion molecule-1 (VCAM-1), intracellular adhesion molecule-1 (ICAM-1), and endothelial-selectin (E-selectin) on the surface of brain endothelial cells. Bigelovin significantly inhibited these in a dose-dependent manner without affecting cell viability. Furthermore, bigelovin suppressed the nuclear factor kappaB (NF-kappaB) promoter-driven luciferase activity, NF-kappaB activation, and degradation of NF-kappaB inhibitor protein alpha (IkappaBalpha). These results indicate that bigelovin inhibits inflammatory monocyte adhesion to endothelial cells and the expression of VCAM-1, ICAM-1, and E-selectin by blocking IkappaBalpha degradation and NF-kappaB activation. PMID:19429369

Nam, Kung-Woo; Oh, Goo Taeg; Seo, Eun-Kyoung; Kim, Kyeong Ho; Koo, Uk; Lee, Sung-Jin; Mar, Woongchon

2009-03-26

252

Regulation of CD4+ T Cells by Pleural Mesothelial Cells via Adhesion Molecule-Dependent Mechanisms in Tuberculous Pleurisy  

PubMed Central

Background Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) have been demonstrated to be expressed on pleural mesothelial cells (PMCs), and to mediate leukocyte adhesion and migration; however, little is known about whether adhesion molecule-dependent mechanisms are involved in the regulation of CD4+ T cells by PMCs in tuberculous pleural effusion (TPE). Methods Expressions of ICAM-1 and VCAM-1 on PMCs, as well as expressions of CD11a and CD29, the counter-receptors for ICAM-1 and VCAM-1, respectively, expressed on CD4+ T cells in TPE were determined using flow cytometry. The immune regulations on adhesion, proliferation, activation, selective expansion of CD4+ helper T cell subgroups exerted by PMCs via adhesion molecule-dependent mechanisms were explored. Results Percentages of ICAM-1-positive and VCAM-1?positive PMCs in TPE were increased compared with PMC line. Interferon-? enhanced fluorescence intensity of ICAM-1, while IL-4 promoted VCAM-1 expression on PMCs. Percentages of CD11ahighCD4+ and CD29highCD4+ T cells in TPE significantly increased as compared with peripheral blood. Prestimulation of PMCs with anti?ICAM-1 or ?VCAM-1 mAb significantly inhibited adhesion, activation, as well as effector regulatory T cell expansion induced by PMCs. Conclusions Our current data showed that adhesion molecule pathways on PMCs regulated adhesion and activation of CD4+ T cells, and selectively promoted the expansion of effector regulatory T cells.

Yuan, Ming-Li; Tong, Zhao-Hui; Jin, Xiao-Guang; Zhang, Jian-Chu; Wang, Xiao-Juan; Ma, Wan-Li; Yin, Wen; Zhou, Qiong; Ye, Hong; Shi, Huan-Zhong

2013-01-01

253

The effect of nanoparticles on the adhesion of epoxy adhesive  

Microsoft Academic Search

In this investigation, the influence of different nanoparticles and surface roughness on the adhesion between epoxy adhesive and steel substrate was primarily investigated. The results of pull-off adhesion tests indicated that nano-Al2O3 of the three kinds of nanoparticles had the most influence on adhesion strength, which was the optimal additive for the epoxy adhesive to improve the adhesion strength. Also,

Lanlan Zhai; Guoping Ling; Jian Li; Youwen Wang

2006-01-01

254

Dietary fat increases solid tumor growth and metastasis of 4T1 murine mammary carcinoma cells and mortality in obesity-resistant BALB/c mice  

PubMed Central

Introduction High-fat diets (HFDs) are known to cause obesity and are associated with breast cancer progression and metastasis. Because obesity is associated with breast cancer progression, it is important to determine whether dietary fat per se stimulates breast cancer progression in the absence of obesity. This study investigated whether an HFD increases breast cancer growth and metastasis, as well as mortality, in obesity-resistant BALB/c mice. Methods The 4-week-old, female BALB/c mice were fed HFD (60% kcal fat) or control diet (CD, 10% kcal fat) for 16 weeks. Subsequently, 4T1 mammary carcinoma cells were injected into the inguinal mammary fat pads of mice fed continuously on their respective diets. Cell-cycle progression, angiogenesis, and immune cells in tumor tissues, proteases and adhesion molecules in the lungs, and serum cytokine levels were analyzed with immunohistochemistry, Western blotting, and enzyme-linked immunosorbent assay (ELISA). In vitro studies were also conducted to evaluate the effects of cytokines on 4T1 cell viability, migration, and adhesion. Results Spleen and gonadal fat-pad weights, tumor weight, the number and volume of tumor nodules in the lung and liver, and tumor-associated mortality were increased in the HFD group, with only slight increases in energy intake and body weight. HF feeding increased macrophage infiltration into adipose tissues, the number of lipid vacuoles and the expression of cyclin-dependent kinase (CDK)2, cyclin D1, cyclin A, Ki67, CD31, CD45, and CD68 in the tumor tissues, and elevated serum levels of complement fragment 5a (C5a), interleukin (IL)-16, macrophage colony-stimulating factor (M-CSF), soluble intercellular adhesion molecule (sICAM)-1, tissue inhibitors of metalloproteinase (TIMP)-1, leptin, and triggering receptor expressed on myeloid cells (TREM)-1. Protein levels of the urokinase-type plasminogen activator, ICAM-1, and vascular cell adhesion molecule-1 were increased, but plasminogen activator inhibitor-1 levels were decreased in the lungs of the HFD group. In vitro assays using 4T1 cells showed that sICAM-1 increased viability; TREM-1, TIMP-1, M-CSF, and sICAM-1 increased migration; and C5a, sICAM-1, IL-16, M-CSF, TIMP-1, and TREM-1 increased adhesion. Conclusions Dietary fat increases mammary tumor growth and metastasis, thereby increasing mortality in obesity-resistant mice.

2011-01-01

255

Bond Properties of Liquid Adhesive.  

National Technical Information Service (NTIS)

Studies were conducted on a liquid adhesive used to bond circuit laminates to rigid plastic components. Areas investigated include: adhesive formulation, factors influencing bond strength, laminate cleaning, and automated adhesive application. (ERA citati...

G. W. Bohnert

1982-01-01

256

Environmentally compliant adhesive joining technology.  

National Technical Information Service (NTIS)

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 proces...

J. S. Tira

1996-01-01

257

Postoperative Peritoneal Adhesions  

PubMed Central

This paper describes an experimental model of peritoneal adhesions, in the rat, based on two relatively minor accidents that may occur during abdominal surgery in man: drying of the serosa, and bleeding. Drying alone had little effect; drying plus bleeding consistently produced adhesions to the dried area. Fresh blood alone produced adhesions between the three membranous structures [omentum and pelvic fat bodies (PFBs)]. The formation of persistent adhesions required whole blood. Preformed clots above a critical size induced adhesions even without previous serosal injury; they were usually captured by the omentum and PFBs. If all three membranous structures were excised, the clots caused visceral adhesions. The protective role of the omentum, its structure, and the mechanism of omental adhesions, are discussed. These findings are relevant to the pathogenesis of post-operative adhesions in man. ImagesFig 3Fig 4Fig 5Fig 6Fig 7Fig 12Fig 13Fig 1Fig 2Fig 14Fig 15Fig 8Fig 9Fig 10Fig 11

Ryan, Graeme B.; Grobety, Jocelyne; Majno, Guido

1971-01-01

258

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

259

High performance conductive adhesives  

Microsoft Academic Search

Isotropic conductive adhesives (ICAs) have been developed as an alternative for traditional tin\\/lead (Sn\\/Pb) solders for electronic applications. Compared to mature soldering technology, conductive adhesive technology is still in its infant stage, therefore, there are some limitations for current commercial ICAs. Two critical limitations are poor impact performance and unstable contact resistance with nonnoble metal finished components. These limitations seriously

Daoqiang Lu; C. P. Wong

1999-01-01

260

Platelet-Collagen Adhesion\\  

Microsoft Academic Search

Univalent antibody fragments prepared from a rabbit antiserum raised against whole human platelets completely inhibited adhesion of platelets to immobilized trimeric collagen in a defined, Mg2+-dependent, adhesion assay. An octylglucoside extract of whole platelets completely neutralized this antibody, and all neutralizing activity bound to immobi- lized wheat germ agglutinin. Further fractionation on concanavalin A gave rise to subfractions that each

PAULA J. SHADLE; SAMUEL H. BARONDES

261

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

262

LEUKOCYTE ADHESION DEFICIENCIES  

Technology Transfer Automated Retrieval System (TEKTRAN)

Aberrations in adhesive mechanisms account for several clinical syndromes that involve an increase in susceptibility to bacterial infection. Leukocyte adhesion deficiency I (LAD I) (MIM 116920) was the first to be defined at a molecular level; it results from mutations in CD18, the beta subunit of b...

263

Development of Phosphorylated Adhesives.  

National Technical Information Service (NTIS)

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 der...

N. Bilow T. W. Giants R. K. Jenkins P. L. Campbell

1983-01-01

264

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

265

NO reduces PMN adhesion to human vascular endothelial cells due to downregulation of ICAM-1 mRNA and surface expression.  

PubMed

Reperfusion damage is largely due to the adherence of polymorphonuclear leukocytes to the endothelium initiated by adhesion molecule upregulation. The reduced endothelial nitric oxide release during ischemia may be involved in the upregulation of intercellular adhesion molecule 1. In this study, we tested if nitric oxide donors suppress polymorphonuclear leukocyte adherence to activated endothelial cells by inhibition of the intercellular adhesion molecule 1 surface expression. Confluent human umbilical vein endothelial cells were stimulated with tumor necrosis factor alpha (300 U/mL) after preincubation with increasing concentrations of the nitric oxide donors CAS 1609 (0.005-5 mM/L) and 3-(4-morpholinyl)-sydnonimine (0.01-1 mM/L). Intercellular adhesion molecule 1 surface expression was measured in a cell surface enzyme-linked immunosorbent assay, intercellular adhesion molecule 1 mRNA by Northern analysis. Human saphenous vein endothelial cells were transfected with the inducible nitric oxide synthase gene and stimulated with tumor necrosis factor alpha (300 U/mL). Fluorescein green-labeled polymorphonuclear leukocytes adhering to activated human umbilical vein endothelial cells/human saphenous vein endothelial cells were quantified by epifluorescent microscopy. The intercellular adhesion molecule 1 surface expression of activated human umbilical vein endothelial cells/human saphenous vein endothelial cells was significantly diminished to 40 to 60% of the maximum after treatment with CAS 1609, 3-(4-morpholinyl)-sydnonimine, or transfection with the inducible nitric oxide synthase gene. Intercellular adhesion molecule 1 mRNA was diminished by CAS 1609 and 3-(4-morpholinyl)-sydnonimine in the same manner. The functional relevance of our data was shown by reduction of polymorphonuclear leukocyte adherence to activated human umbilical vein endothelial cells/human saphenous vein endothelial cells following treatment with CAS 1609 and 3-(4-morpholinyl)-sydnonimine or transfection with inducible nitric oxide synthase. Tumor necrosis factor-induced polymorphonuclear leukocyte adherence was abolished by blocking antibody against intercellular adhesion molecule 1. Thus, exogenous or endogenous substitution of nitric oxide diminishes the expression of endothelial intercellular adhesion molecule 1 and its mRNA following tumor necrosis factor alpha stimulation. This results in a reduced polymorphonuclear leukocyte adherence to activated endothelium. PMID:10680642

Lindemann, S; Sharafi, M; Spiecker, M; Buerke, M; Fisch, A; Grosser, T; Veit, K; Gierer, C; Ibe, W; Meyer, J; Darius, H

2000-02-01

266

Altered expression of cell adhesion molecules in uninvolved gut in inflammatory bowel disease.  

PubMed Central

Adhesion of circulating cells to vascular endothelium occurs in the early phase of inflammation, and is mediated by specific cell adhesion molecules. Many such adhesion molecules are increased in inflamed regions of ulcerative colitis (UC) and Crohn's disease (CD) but there is limited knowledge of their expression in the uninvolved gut, adjacent to inflammation. We investigated immunohistochemically the expression of platelet endothelial cell adhesion molecule-1 (PECAM-1), intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-1 (LFA-1) on resected specimens taken at a distance of 2-4 cm from the inflamed area and without histological signs of inflammation. Compared with normal gut, we found (i) a significant increase of PECAM-1-positive vessels in the mucosa of uninvolved UC (149.0 +/- 24.1 vessels/mm2 (mean +/- s.d.); normal colon = 123.1 +/- 21.6; P = 0.004); (ii) a significant decrease of ICAM-1-positive vessels in uninvolved CD (111.9 +/- 22.6 vessels/mm2; normal ileum = 136.9 +/- 27.6; P = 0.04); and (iii) a moderate but statistically insignificant increase of LFA-1-positive cells in the mucosa of uninvolved UC and Crohn's ileitis. This altered expression of cell adhesion molecules may contribute to the early lesion in inflammatory bowel disease and provide new therapeutic opportunities. Images Fig. 1 Fig. 2

Schuermann, G M; Aber-Bishop, A E; Facer, P; Lee, J C; Rampton, D S; Dore, C J; Polak, J M

1993-01-01

267

Adhesion of Polymer Vesicles  

NASA Astrophysics Data System (ADS)

The adhesion and bending modulus of polybutadiene-poly(ethylene oxide) block copolymer vesicles made from a bidisperse mixture of polymers is measured using micropipette aspiration. The adhesion energy between biotinylated vesicles and avidin beads is modeled by incorporating the extension of the adhesive ligands above the surface brush of the vesicle according to the blob model of bidisperse polymer mixtures of Komura and Safran assuming the polymer brush at the surface of the vesicle is compact. The same model accurately reproduces the scaling of the bending modulus with polymer composition.

Lin, John J.; Bates, Frank S.; Hammer, Daniel A.; Silas, James A.

2005-07-01

268

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

269

Focal adhesions in osteoneogenesis  

PubMed Central

As materials technology and the field of tissue engineering advances, the role of cellular adhesive mechanisms, in particular the interactions with implantable devices, becomes more relevant in both research and clinical practice. A key tenet of medical device technology is to use the exquisite ability of biological systems to respond to the material surface or chemical stimuli in order to help develop next-generation biomaterials. The focus of this review is on recent studies and developments concerning focal adhesion formation in osteoneogenesis, with an emphasis on the influence of synthetic constructs on integrin mediated cellular adhesion and function.

Biggs, M.J.P; Dalby, M.J

2010-01-01

270

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

271

POST, partner of stromal interaction molecule 1 (STIM1), targets STIM1 to multiple transporters  

PubMed Central

Specialized proteins in the plasma membrane, endoplasmic reticulum (ER), and mitochondria tightly regulate intracellular calcium. A unique mechanism called store-operated calcium entry is activated when ER calcium is depleted, serving to restore intra-ER calcium levels. An ER calcium sensor, stromal interaction molecule 1 (STIM1), translocates within the ER membrane upon store depletion to the juxtaplasma membrane domain, where it interacts with intracellular domains of a highly calcium-selective plasma membrane ion channel, Orai1. STIM1 gates Orai1, allowing calcium to enter the cytoplasm, where it repletes the ER store via calcium-ATPases pumps. Here, we performed affinity purification of Orai1 from Jurkat cells to identify partner of STIM1 (POST), a 10-transmembrane–spanning segment protein of unknown function. The protein is located in the plasma membrane and ER. POST-Orai1 binding is store depletion-independent. On store depletion, the protein binds STIM1 and moves within the ER to localize near the cell membrane. This protein, TMEM20 (POST), does not affect store-operated calcium entry but does reduce plasma membrane Ca2+ pump activity. Store depletion promotes STIM1–POST complex binding to smooth ER and plasma membrane Ca2+ ATPases (SERCAs and PMCAs, respectively), Na/K-ATPase, as well as to the nuclear transporters, importins-? and exportins.

Krapivinsky, Grigory; Krapivinsky, Luba; Stotz, Stephanie C.; Manasian, Yunona; Clapham, David E.

2011-01-01

272

Kidney injury molecule-1 is an early biomarker of cadmium nephrotoxicity  

PubMed Central

Cadmium (Cd) exposure results in injury to the proximal tubule characterized by polyuria and proteinuria. Kidney injury molecule-1 (Kim-1) is a transmembrane glycoprotein not normally detected in the mature kidney, but is upregulated and shed into the urine following nephrotoxic injury. In this study, we determine if Kim-1 might be a useful early biomarker of Cd nephrotoxicity. Male Sprague-Dawley rats were given daily injections of Cd for up to 12 weeks. Weekly urine samples were analyzed for Kim-1, protein, creatinine, metallothionein, and Clara cell protein CC-16. Significant levels of Kim-1 were detected in the urine by 6 weeks and continued to increase throughout the treatment period. This appearance of Kim-1 occurred 4-5 weeks before the onset of proteinuria, and 1-3 weeks before the appearance of metallothionein and CC-16. Higher doses of Cd gave rise to higher Kim-1 excretion. Reverse transcriptase-polymerase chain reaction (RT-PCR) expression analysis showed that Kim-1 transcript levels were increased after 6 weeks at the low dose of Cd. Immunohistochemical analysis showed that Kim-1 was present in proximal tubule cells of the Cd-treated rats. Our results suggest that Kim-1 may be a useful biomarker of early stages of Cd-induced proximal tubule injury.

Prozialeck, WC; Vaidya, VS; Liu, J; Waalkes, MP; Edwards, JR; Lamar, PC; Bernard, AM; Dumont, X; Bonventre, JV

2009-01-01

273

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

274

Adhesive for composite bonding.  

National Technical Information Service (NTIS)

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 attachm...

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

1989-01-01

275

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 is discussed. The process for making the improved adhesiv...

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

1981-01-01

276

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

277

Effect of soy nuts on adhesion molecules and markers of inflammation in hypertensive and normotensive postmenopausal women.  

PubMed

Recently, it was shown that substituting soy nuts for nonsoy protein in a therapeutic lifestyle change (TLC) diet lowered systolic and diastolic blood pressure by 9.9% and 6.8%, respectively, in postmenopausal women with hypertension and by 5.2% and 2.9%, respectively, in normotensive postmenopausal women. In this study, to examine mechanisms for these reductions, markers of inflammation were measured, including soluble vascular cell adhesion molecule-1, soluble intercellular adhesion molecule-1, C-reactive protein, interleukin-6, and matrix metalloproteinase-9. Sixty healthy postmenopausal women (48 normotensive and 12 with hypertension) were randomized in a crossover design to a TLC diet alone or a TLC diet in which 0.5 cups of soy nuts (25 g soy protein and 101 mg aglycone isoflavones) replaced 25 g of nonsoy protein daily. Each diet was followed for 8 weeks. Compared with the TLC diet alone, levels of soluble vascular cell adhesion molecule-1 were significantly lower on the soy diet in women with hypertension (623.6 +/- 153.8 vs 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 C-reactive protein in normotensive women. No effect on levels of soluble intercellular adhesion molecule-1, interleukin-6, or matrix metalloproteinase-9 was observed. In conclusion, the reduction in soluble vascular cell adhesion molecule-1 with soy nuts in women with hypertension suggests an improvement in endothelial function that may reflect an overall improvement in the underlying inflammatory process underlying atherosclerosis. PMID:18572041

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

2008-04-16

278

[Prevention of postoperative adhesions].  

PubMed

Postoperative adhesions represent a common consequence in patients who underwent abdominal or pelvic surgery. Such adhesions can be asymptomatic, but they can cause complications such as chronic abdomino-pelvic pain, secondary infertility, an increase in bowel obstruction risk and more complexity for future surgery, including longer surgery times and an increase in morbidity. Normally, adhesions appear after offences against the peritoneum, causing flogosys, and develop both in new sites, previously not involved, and in sites already interested in adhesiolysis. Previous laparotomy is an important risk factor, as after laparatomy a minimum of 93% of patients present adhesions during a following surgery. Furthermore, the rate of recurrence after adhesiolysis is 85%. Among several strategies employed, valid prevention methods are: using minimally invasive surgery techniques, reducing the incision area, containing tissue dehydration during surgery and an accurate hemostasis. Also, for preventing and reducing adhesions, the usage of NSAIDs, fibrinolytics and anticoagulants, as well as the application of substances acting as a physical barrier, have been proposed. Recently, crystalloid solutions have been introduced, using the hydro-flotation principle for intraperitoneal organs. This research aims to analyze causes and epidemiology for postoperative adhesions, with particular regard to gynecological operations and to describe and compare the means available to prevent them. PMID:19204662

Palaia, I; Boni, T; Angioli, R; Muzii, L; Polidori, N F; Andrei, N F; Musella, A; De Oronzo, M A; Guzzo, F; Benedetti Panici, P

2009-02-01

279

Prognostic impact of in vivo soluble cell adhesion molecules in metastatic renal cell carcinoma  

Microsoft Academic Search

The purpose of the study was to determine prognostic significance of pretreatment serum levels of different molecules involved in cell to cell interactions along with other clinical parameters in patients with metastatic renal cell carcinoma. sICAM-1, sVCAM-1 and sELAM-1 serum levels were determined by ELISA assays in sera from 99 patients with histologically confirmed progressive metastatic renal cell carcinoma prior

R Hoffmann; A Franzke; J Buer; S Sel; K Oevermann; A Duensing; M Probst; S Duensing; H Kirchner; A Ganser; J Atzpodien

1999-01-01

280

Anti-inflammatory drugs and endothelial cell adhesion molecule expression in murine vascular beds  

PubMed Central

Background—Inflammatory bowel diseases (IBD) are characterised by an intense infiltration of leucocytes that is mediated by adhesion molecules expressed on the surface of activated endothelial cells. ?Aims—To determine whether drugs used in the treatment of IBD, specifically dexamethasone (DEX), 5-aminosalicylic acid (5-ASA), methotrexate (MTX), and 6-mercaptopurine (6-MP), alter the expression of endothelial cell adhesion molecules (ECAMs). ?Methods—The expression of P-selectin, E-selectin, intercellular adhesion molecule 1 (ICAM-1), and vascular CAM 1(VCAM-1) in different vascular beds of C57Bl/6J mice was measured using the dual radiolabelled monoclonal antibody technique. ?Results—Lipopolysaccharide (LPS) elicited a profound increase in the expression of all ECAMs in the mesentery, small intestine, caecum, and distal colon. The LPS induced increase in CAM expression was not significantly affected by prior treatment with either MTX or 6-MP. However, pretreatment with either DEX or 5-ASA significantly attenuated LPS induced increases in expression of P- and E-selectin, and VCAM-1 in the majority of tissues evaluated. DEX also blunted the LPS induced increase in ICAM-1 expression in the caecum and distal colon. DEX, but not 5-ASA, largely abolished the rise in plasma tumour necrosis factor ? elicited by LPS. ?Conclusions—These findings suggest that DEX and 5-ASA may exert their beneficial therapeutic action in IBD, at least in part, by inhibiting the expression of ECAMs which mediate leucocyte adhesion and transmigration in the microvasculature. ?? Keywords: P-selectin; E-selectin; intercellular adhesion molecule 1; vascular cell adhesion molecule 1; dexamethasone; 5-aminosalicylic acid

Mori, N; Horie, Y; Gerritsen, M; Anderson, D; Granger, D

1999-01-01

281

Susceptibility of HIV Type 1 to the Fusion Inhibitor T?20 Is Reduced on Insertion of Host Intercellular Adhesion Molecule 1 in the Virus Membrane  

Microsoft Academic Search

Background. T-20 is a synthetic peptide that targets and blocks the entry of human immunodeficiency virus (HIV)-1 inside target cells. Data from clinical studies have shown that primary HIV-1 variants display a broad range of susceptibilities to T-20 that are mainly caused by mutations in the N-terminal heptad repeat of gp41 and by other determinants, such as envelope and coreceptor

Yannick Beauséjour

2004-01-01

282

Intercellular adhesion molecule 1 gene K469E polymorphism is associated with coronary heart disease risk: a meta-analysis involving 12 studies.  

PubMed

Coronary atherosclerosis is a leading cause of coronary heart disease (CHD). Atherosclerotic lesion is a complex polygenic disease in which gene-environment interactions play a critical role in disease onset and progression. The ICAM1 gene-E469K polymorphism has been reported to be associated with CHD, but results were conflicting. A systematic review and meta-analysis of the published studies were performed to gain a clearer understanding of this association. The PubMed, Embase, and CNKI databases were searched for case-control studies published up to August 2011. Data were extracted and pooled odds ratios (OR) with 95% confidence intervals (CI) were calculated. Twelve eligible studies, comprising 2,157 cases and 1,952 controls, were included in the meta-analysis. The pooled result showed that the ICAM1 gene-E469K polymorphism was significantly associated with an increased risk of CHD (OR = 1.496, 95% CI = 1.363-1.642, for the allele K vs. allele E; OR = 1.919, 95% CI = 11.635-2.253, for the K allele carriers vs. EE). Subgroup analysis supported the results in the Asian populations and in the Caucasian populations. This meta-analysis suggests that the ICAM1 gene K469E polymorphism is associated with CHD risk and the K allele is a more significant risk factor for developing CHD among Asian and Caucasians populations. PMID:22203486

Ji, Ya-Nan; Wang, Qin; Zhan, Ping

2011-12-28

283

Functional Implication of the Hydrolysis of Platelet Endothelial Cell Adhesion Molecule 1 (CD31) by Gingipains of Porphyromonas gingivalis for the Pathology of Periodontal Disease  

Microsoft Academic Search

Received 13 September 2004\\/Returned for modification 26 October 2004\\/Accepted 8 November 2004 Periodontitis is a response of highly vascularized tissues to the adjacent microflora of dental plaque. Progressive disease has been related to consortia of anaerobic bacteria, with the gram-negative organism Porphyromonas gingivalis particularly implicated. The gingipains, comprising a group of cysteine proteinases and associated hemagglutinin domains, are major virulence

Peter L. W. Yun; Arthur A. Decarlo; Cheryl C. Chapple; Neil Hunter

2005-01-01

284

Keishibukuryogan (Gui-Zhi-Fu-Ling-Wan), a Kampo Formula, Decreases Disease Activity and Soluble Vascular Adhesion Molecule1 in Patients with Rheumatoid Arthritis  

Microsoft Academic Search

An increasing death rate due to cardiovascular disease in patients with rheumatoid arthritis (RA) has been reported. Keishibukuryogan (KBG) is a traditional Chinese\\/Japanese (Kampo) formula that has been administered to patients with blood stagnation, e.g. thrombotic disease and atherosclerosis. The objective of this study was to evaluate the efficacy of KBG on disease activity and endothelial dysfunction in RA patients.

Kazuya Nozaki; Hiroaki Hikiami; Hirozo Goto; Takako Nakagawa; Naotoshi Shibahara; Yutaka Shimada

2006-01-01

285

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

286

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

2013-08-05

287

Effects of 17beta-estradiol on cytokine-induced endothelial cell adhesion molecule expression.  

PubMed Central

One of the earliest events in atherosclerosis is interaction of circulating mononuclear leukocytes and the endothelium. Endothelial cell (EC) activation by cytokines results in expression of adhesion molecules and production of chemotactic factors, augmenting leukocyte adhesion and recruitment, respectively. The incidence of atherosclerosis in premenopausal women is significantly less than that observed in age-matched males with similar risk profiles. Because estrogen has gene regulatory effects, we investigated whether 17beta-estradiol (E2) can inhibit cytokine-mediated EC adhesion molecule transcriptional activation. Cultured human umbilical vein EC (estrogen receptor-positive) were propagated in gonadal hormone-free medium and were E2-pretreated for 48 h before IL-1 activation. Detected by FACS analysis, E2 strongly (60-80%) inhibited IL-1-mediated membrane E-selectin and vascular cell adhesion molecule-1 induction, and intercellular adhesion molecule-1 hyperinduction. 17alpha-estradiol (an inactive E2 stereoisomer) had no effect. This inhibition correlated with similar reductions in steady state-induced E-selectin mRNA levels, and was abrogated by the E2 antagonist ICI 164,384, demonstrating a specific, estrogen receptor-mediated effect. Nuclear run-offs confirmed suppression at the transcriptional level. The implications of these results for the cardiovascular protective role of estrogen are discussed.

Caulin-Glaser, T; Watson, C A; Pardi, R; Bender, J R

1996-01-01

288

Role of leucocyte adhesion molecules in aminonucleoside of puromycin (PAN)-associated interstitial nephritis.  

PubMed

Rats receiving a single dose (10 mg/l00 g body wt) of PAN develop severe proteinuria and acute interstitial nephritis. To investigate the mechanisms involved in interstitial leucocyte accumulation, we examined the expression of adhesion molecules on kidney tissue sections as well as on endothelial cell cultures. We also performed in vivo treatments with antibodies against adhesion molecules. Enhanced expression of intercellular adhesion molecule-1 (ICAM-1) was found on day 7 of the disease, when interstitial nephritis was first detected. Also, rat endothelial cells in culture showed maximal expression of ICAM-1 in the presence of 10(-9) - 10(-11) M PAN. Adhesion of peripheral blood mononuclear cells (PBMC) on kidney sections from PAN-treated rats was highest on day 7 (3.05 +/- 0.7 (mean +/- s.e.m.); controls 0.75 +/- 0.5). Such increased adhesion was notably blocked after PAN-treated rat kidney sections were incubated with anti-ICAM-1 MoAb (0.9 +/- 0.4). In addition, adhesiveness of PBMC to PAN-stimulated endothelial cells in culture was enhanced (25 +/- 2.5%; non-stimulated cells 13 +/- 3.1%). The addition of specific MoAbs against ICAM-1 and lymphocyte function-associated antigen-1 (LFA-1) produced a high blockage of adhesiveness induced by exposure to PAN (inhibition 58 +/- 3%; non-stimulated cells 40 +/- 7%). Simultaneous administration to PAN-treated rats of anti-LFA-1 and anti-ICAM-1 MoAbs reduced the number of interstitial cells by 70% compared with the 30% of reduction obtained when anti-very late antigen-4 (VLA-4) MoAb and anti-vascular cell adhesion molecule-1 (VCAM-1) antibodies were used. Our results suggest that the LFA-1/ICAM-1 pathway plays a principal role in the interstitial nephritis occurring in rats with PAN-nephrosis. PMID:9097915

Martín, A; Escudero, E; Mampaso, F

1997-04-01

289

Combinatorial Investigations of Polymer Adhesion  

NSDL National Science Digital Library

In this work, we introduce a combinatorial technique that can be used to investigate adhesive interactions between a polymer and either another polymer, a ceramic, or a metal. The primary goal in the development of this technique is to design a high-throughput, parallel processing adhesion test that allows the adhesive strength dependence on multivariable environments to be determined. This combinatorial polymer adhesion test will provide qualitative and quantitative data used to determine absolute measures of adhesion as a function of the multidimensional parameter space. These results will aid industrial screening for optimal adhesives, as well as provide a unique tool for gaining a fundamental understanding of polymer adhesion. We investigate the temperature and thickness dependence of the self-adhesion of polystyrene (PS) and the adhesion between PS and poly(dimethylsiloxane) (PDMS) for demonstration of concept.

Crosby, Alfred; Karim, Alamgir; Amis, Eric

2001-01-01

290

Homocysteine, circulating vascular cell adhesion molecule and carotid atherosclerosis in postmenopausal vegetarian women and omnivores  

Microsoft Academic Search

Since the adoption of vegetarian diets as a healthy lifestyle has become popular, the cardiovascular effects of long-term vegetarianism need to be explored. The present study aimed to compare the presence and severity of carotid atherosclerosis (CA), and the blood levels of Vitamin B12, homocysteine (Hcy) and soluble vascular cell adhesion molecule-1 (sVCAM-1) between 57 healthy postmenopausal vegetarians and 61

Ta-Chen Su; Jiann-Shing Jeng; Jung-Der Wang; Pao-Ling Torng; Sue-Joan Chang; Chen-Fang Chen; Chiau-Suong Liau

2006-01-01

291

Epithelial Cell Adhesion Molecule  

PubMed Central

The epithelial cell adhesion molecule (EpCAM, CD326) is a glycoprotein of ?40 kd that was originally identified as a marker for carcinoma, attributable to its high expression on rapidly proliferating tumors of epithelial origin. Normal epithelia express EpCAM at a variable but generally lower level than carcinoma cells. In early studies, EpCAM was proposed to be a cell-cell adhesion molecule. However, recent insights revealed a more versatile role for EpCAM that is not limited only to cell adhesion but includes diverse processes such as signaling, cell migration, proliferation, and differentiation. Cell surface expression of EpCAM may actually prevent cell-cell adhesion. Here, we provide a comprehensive review of the current knowledge on EpCAM biology in relation to other cell adhesion molecules. We discuss the implications of the newly identified functions of EpCAM in view of its prognostic relevance in carcinoma, inflammatory pathophysiology, and tissue development and regeneration as well as its role in normal epithelial homeostasis.

Trzpis, Monika; McLaughlin, Pamela M.J.; de Leij, Lou M.F.H.; Harmsen, Martin C.

2007-01-01

292

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

293

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

294

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

295

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

296

Timer cover adhesive optimization  

SciTech Connect

The implementation of PROCODE as the data acquisition system for processing timers has required some modifications to the method of identifying timer assemblies. PROCODE requires machine-readable labelling of the assemblies. This report describes a series of experiments to find an adhesive that would keep labels attached to timers regardless of the condition of their surface when the label was applied and regardless of the heat, vibration, and shock they endured afterwards. The effect of the variation of these experimental factors on the performance of the adhesive was determined by using a Taguchi experimental design.

Carleton, J.J. II.

1992-03-17

297

The Chemistry of Structural Adhesives: Epoxy, Urethane, and Acrylic Adhesives  

NASA Astrophysics Data System (ADS)

Adhesives have been used successfully in a variety of applications for centuries. Today, adhesives are more important than ever in our daily lives, and their usefulness is increasing rapidly. In the past few decades there have been significant advances in materials and in bonding technology. People now routinely trust their fortunes and their lives to adhesively bonded structures and rarely think about it.

Zalucha, Denis J.; Abbey, Kirk J.

298

The adhesion cascade and anti-adhesion therapy: an overview  

Microsoft Academic Search

Investigations in the past decade have greatly advanced our knowledge of both the molecular pathways of leukocyte adhesion and the contribution of leukocytes to a wide range of organ injuries. As a result, it is now possible to separate the leukocyte adhesion\\/emigration process into discrete steps, defined by specific molecular interactions. The multistep process of leukocyte-endothelial adhesion (cell activation, leukocyte

Sam R. Sharar; Robert K. Winn; John M. Harlan

1995-01-01

299

Expression of stress proteins, adhesion molecules, and interleukin-8 in endothelial cells after preservation and reoxygenation.  

PubMed

Endothelial activation is a central feature of preservation-induced allograft injury. The present study aims at a quantitative assessment of stress proteins, adhesion molecules, and interleukin-8 in a cell culture-based model of organ preservation. Human umbilical vein endothelial cells were exposed to cold, hypoxic storage in University of Wisconsin (UW), histidine-tryptophane-ketoglutarate (HTK), and EuroCollins solutions for 8 h with subsequent rewarming/reoxygenation (rew/reox) for 1 and 4 h. A cell-based ELISA was designed for detection of heat shock proteins (HSP) 60 and 70, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and endothelial leukocyte adhesion molecule-1 (ELAM-1). Immunohistochemical staining was performed for comparison. Interleukin-8 was quantified by ELISA. HSP 70 was expressed after cold storage in HTK and EuroCollins solution and after rew/reox in all groups. A constitutive expression of HSP 60 was observed with further upregulation after rew/reox following cold storage in all experimental groups. ICAM-1 was clearly upregulated, but VCAM-1 showed only weak expression after cold storage and rew/reox. ELAM-1 was detectable in minimal amounts after cold storage but was considerably upregulated after 4 h of rew/reox. A significant increase of interleukin-8 release could be found after 4 h of rew/reox following storage in EuroCollins solution. Expression of stress proteins can be considered as a new parameter of preservation-associated endothelial activation. Apart from possible protective effects, allograft vasculopathy could be in part a consequence of the antigeneic potential of heat shock proteins connected with effects caused by adhesion molecules and inflammatory cytokines. PMID:10191034

Eberl, T; Amberger, A; Herold, M; Hengster, P; Steurer, W; Hochleitner, B W; Gnaiger, E; Margreiter, R

1999-03-01

300

Individual and Neighborhood Socioeconomic Status and Inflammation in Mexican-American Women: What is the Role of Obesity?  

PubMed Central

Objective Inflammation may represent a biological mechanism underlying associations of socioeconomic status (SES) with cardiovascular disease (CVD). The current study examined relationships of individual and neighborhood SES with inflammatory markers in Mexican-American women and evaluated contributions of obesity and related heath behaviors to these associations. Methods A random sample of 284 Mexican-American women (mean age 49.74 years) was recruited from socioeconomically diverse South San Diego communities. Women completed measures of sociodemographic characteristics and health behaviors, and a physical examination with fasting blood draw for assay of plasma C-reactive-protein (CRP), interleukin-6 (IL-6), and soluble intercellular adhesion molecule-1 (sICAM-1). Neighborhood SES was extracted from the US Census Bureau 2000 database. Results In multilevel models, a one-standard deviation (SD) higher individual and neighborhood SES related to a 27.35% and 23.56% lower CRP (ps < .01), a 7.04% and 5.32% lower sICAM-1 (ps < .05), and a 10.46% (p < .05) and 2.40% lower IL-6 level (NS), respectively. Controlling for individual SES, a one-SD higher neighborhood SES related to a 18.05% lower CRP (p = .07); there was no unique effect of neighborhood SES for IL-6 or sICAM-1. Differences in body mass index, waist circumference, and dietary fat consumption contributed significantly to SES-inflammation associations. Conclusions The findings support a link between SES and inflammatory markers in Mexican-American women, and implicate obesity and dietary fat in these associations. Additional effects of neighborhood SES were not statistically significant. These findings should be viewed tentatively because the relatively small sample size limits the evaluation of multiple contextual factors.

Gallo, Linda C.; Fortmann, Addie L.; de los Monteros, Karla Espinosa; Mills, Paul J.; Barrett-Connor, Elizabeth; Roesch, Scott C.; Matthews, Karen A.

2012-01-01

301

Serum interleukin-18 and soluble tumour necrosis factor receptor 2 are associated with disease severity in patients with paracoccidioidomycosis  

PubMed Central

Interleukin (IL)-18 is a proinflammatory cytokine of the IL-1 superfamily that exhibits broad functional effects in innate and acquired immune responses and which has been found in high levels in several chronic inflammatory and autoimmune diseases. Over-expression of IL-18 may promote early resolution of infection or could promote a detrimental exaggerated immune response. The aim of this study was to determine serum levels of IL-18 and other inflammatory mediators [IL-12, soluble intercellular adhesion molecule 1 (sICAM-1), soluble tumour necrosis factor receptor 1 (TNF-RI), sTNF-RII, CXC chemokine ligand 9 (CXCL9), CXCL10] at baseline and after anti-fungal therapy in serum from patients with juvenile (JF) and adult (AF) forms of paracoccidioidomycosis (PCM), as well as in healthy controls (C), and to assess their possible relationships to the severity of disease. IL-18 and sTNF-RII levels in patients with the JF of PCM were significantly higher than those in the AF and controls. In relation to sICAM-1, no difference was observed between JF and AF patients but both presented higher levels than controls. sTNF-RI levels were higher in patients with PCM than in controls, and significantly higher concentrations were detected in AF patients compared to JF patients. Moreover, IL-12 and chemokines CXCL9 and CXCL10 were also higher in patients than in controls. In JF patients IL-18 levels correlated significantly with sICAM-1 (r = 0·62, P < 0·0001), sTNF-RI (r = 0·63, P < 0·0001), sTNF-RII (r = 0·51, P = 0·02), as well as with clinical severity. The results suggest the value of serum IL-18 and sTNF-Rs levels as a parameter of PCM severity and may support a possible role for them in the pathogenesis of the disease.

Corvino, C L; Mamoni, R L; Fagundes, G Z Z; Blotta, M H S L

2007-01-01

302

Dynamics of increased neutrophil adhesion to ICAM-1 after contacting immobilized IL-8.  

PubMed

Changing affinity of beta(2)-integrins on neutrophils for their ligands on endothelium is a critical, regulated step in the inflammatory response. In this report, the dynamics of the neutrophil response to the inflammatory chemokine interleukin-8 (IL-8) is examined. Human IL-8 was immobilized on beads and brought into contact with neutrophils selected from whole blood samples. Resulting changes in cellular adhesion were assessed by measuring the adhesion frequency between a human neutrophil and a bead coated with the endothelial ligand ICAM-1 (intercellular adhesion molecule-1). Cells engulfed the IL-8 coated beads within a few tens of seconds, and most of the cells exhibited an increase in adhesion to ICAM-1 after approximately 5 to 10 min of contact with IL-8 at room temperature (3 to 5 min at 37 degrees C). Neither monocyte chemotactic protein-1 (MCP-1) nor anti-CD45-coated beads caused any changes in adhesion to ICAM-1. IL-8 induced adhesion was blocked by antibody against CD18. At lower surface density of chemokine, approximately 20% of IL-8 coated beads adhered but were not engulfed by the cells, although the increase in adhesion for ICAM-1 was still effected. Heterogeneity in the cellular response and variability between donors was also noted. PMID:17029031

Lomakina, Elena B; Waugh, Richard E

2006-09-20

303

Recent Advances in Adhesion Prevention  

Microsoft Academic Search

Use of adhesion prevention adjuvants has become the standard of practice following gynecologic as well as general surgery\\u000a [1–3]. The frequent occurrence of adhesions after peritoneal cavity surgery and clinical consequences of adhesions, including\\u000a increased rates of reoperation, postoperative bowel obstruction, infertility, and chronic pelvic pain, which markedly increase\\u000a healthcare costs, make prevention of adhesions a major contributor to successful

Gere S. diZerega; Matthias Korell

304

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

305

Adhesion molecules and receptors  

Technology Transfer Automated Retrieval System (TEKTRAN)

Adhesion molecules are necessary for leukocyte trafficking and differentiation. They serve to initiate cell-cell interactions under conditions of shear, and they sustain the cell-cell and cell-matrix interactions needed for cellular locomotion. They also can serve directly as signaling molecules act...

306

Electrically controlled DNA adhesion  

Microsoft Academic Search

The ability to control the interaction of polyelectrolytes, such as DNA or proteins, with charged surfaces is of pivotal importance for a multitude of biotechnological applications. Previously, we measured the desorption forces of single polymers on charged surfaces using an atomic force microscope. Here, we show that the adhesion of DNA on gold electrodes modified with self-assembled monolayers can be

Matthias Erdmann; Ralf David; Ann Fornof; Hermann E. Gaub

2010-01-01

307

Adhesion between nanoparticles  

Microsoft Academic Search

A study of the contact and adhesion between panicles with clean surfaces (free from oxide and other contamination) is important but increasingly more difficult to perform as the particle size is reduced to a nanoscale. A reproducible way of finding such contacts between a large number of nanoparticles has been developed. Cobalt particles within the size range 5–200 nm have

Y. Yao; A. R. Thölén

1999-01-01

308

Adhesion of Nanoparticles  

NASA Astrophysics Data System (ADS)

We have developed a new model of nanoparticle adhesion which explicitly takes into account the change in the nanoparticle surface energy. Using combination of the molecular dynamics simulations and theoretical calculations we have showed that the deformation of the adsorbed nanoparticles is a function of the dimensionless parameter ??( GR )-2/3W-1/3, where G is the particle shear modulus, R is the initial particle radius, ? is the polymer interfacial energy, and W is the particle work of adhesion. In the case of small values of the parameter ?<0.1, which is usually the case for strongly cross-linked large nanoparticles, the particle deformation can be described in the framework of the classical Johnson, Kendall, and Roberts (JKR) theory. However, we observed a significant deviation from the classical JKR theory in the case of the weakly cross-linked nanoparticles that experience large shape deformations upon particle adhesion. In this case the interfacial energy of the nanoparticle plays an important role controlling nanoparticle deformation. Our model of the nanoparticle adhesion is in a very good agreement with the simulation results and provides a new universal scaling relationship for nanoparticle deformation as a function of the system parameters.

Carrillo, Jan-Michael; Raphael, Elie; Dobrynin, Andrey

2011-03-01

309

Graphene Blister Adhesion Mechanics  

NASA Astrophysics Data System (ADS)

We describe graphene blister configurations to study the elasticity of mono- and multi-layer graphene as well as the adhesion of the blister to an SiO2 substrate. We create blisters by depositing graphene on a chip containing etched cavities of a prescribed volume. The chip is placed in a high-pressure chamber where the cavities are charged to a prescribed pressure. When the chip is removed from the chamber the pressure difference across the membrane causes it to bulge, while the number of gas molecules in the chamber remains constant. As the pressure is increased the membrane continues to bulge and at a critical pressure can delaminate (in a stable or unstable manner) permitting extraction of the adhesion energy from a combination of theory and measurements of the deformed blister configuration. We describe these experiments and develop a thermodynamic model of the system that identifies interesting nonlinear effects as the membranes deform including instabilities, delamination, and adhesion hysteresis, depending on the configurational parameters. We use the theory and experiments together to determine for the first time the adhesion energy between graphene and SiO2, as well as explore the interesting mechanics that occur.

Bodetti, Narasimha; Koenig, Steven; Xiao, Jianliang; Bunch, Scott; Dunn, Martin

2012-02-01

310

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

311

Electrical aging of adhesive  

Microsoft Academic Search

Insulating reliability between adjacent leads formed on organic material is an important problem for printed circuits. This problem was investigated in connection with insulator deterioration between copper conductors exposed to high temperature and high humidity under fairly high electric fields in comparison with actual operating conditions. The investigation was performed on a copper foil laminated to a thermoset adhesive coated

H. Narushima; Y. Tsukamoto; J. Koshimura

1989-01-01

312

Adhesiveness and Stickiness\\  

Microsoft Academic Search

SUMMARY For the purposes of this report, adhesiveness was defined as that force which resists the mechanical separation of attached pairs of cells, and stickiness as the tendency of cells to cling to a foreign substrate; in the present experiments the substrate employed was glass. The cells selected for study were from the normal rabbit epiderm and the V2 rabbit

DALE REX COMAN

313

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

2013-05-17

314

The Adhesion of Barnacles  

Microsoft Academic Search

Adhesives for permanent attachment of barnacles are secreted at two stages in the life history. The settlement stage larva exudes a quantity of cement (cyprid cement) from the paired cement glands onto the substratum and this envelops the attachment organs. The permanently attached larva then metamorphoses to the juvenile and after a short growth interval, during which the juvenile is

Graham Walker

1981-01-01

315

Osteoblast adhesion on biomaterials  

Microsoft Academic Search

The development of tissue engineering in the field of orthopaedic surgery is now booming. Two fields of research in particular are emerging: the association of osteo-inductive factors with implantable materials; and the association of osteogenic stem cells with these materials (hybrid materials). In both cases, an understanding of the phenomena of cell adhesion and, in particular, understanding of the proteins

K. Anselme

2000-01-01

316

Thioredoxin1 Downregulates Oxidized Low-Density Lipoprotein-Induced Adhesion Molecule Expression via Smad3 Protein  

PubMed Central

Atherosclerosis is a chronic inflammation disease that is initiated by endothelial cell injury. Oxidized low-density lipoprotein (ox-LDL) is directly associated with chronic vascular inflammation. To understand whether thioredoxin1 (Trx1) participates in an antiinflammatory defense mechanism in atherosclerosis, we investigated the effect of Trx1 on the expression of two adhesion molecules, vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1), in human umbilical vein endothelial cells (HUVECs). Thioredoxin1 and dominant-negative mutant thioredoxin1 (TD) were transiently overexpressed using adenovirus vector gene transfer. Our data showed that Trx1 overexpression suppressed ox-LDL-induced adhesion molecule expression in HUVECs. The overexpression of Trx1 promoted ox-LDL-induced Smad3 phosphorylation and nuclear translocation. A co-immunoprecipitation assay indicated that Smad3 continued to interact with Trx1 with or without ox-LDL stimulation. These results suggest that Trx1 inherently suppresses VCAM-1 and ICAM-1 expression in vascular endothelia and may prevent the initiation of atherosclerosis by attenuating adhesion molecule expression. The enhancement of Smad3 phosphorylation and nuclear expression appears to be primarily responsible for the Trx1-induced downregulation of adhesion molecules.

Chen, Beidong; Wang, Wendong; Shen, Tao; Qi, Ruomei

2013-01-01

317

[Tumor metastasis and adhesion molecules].  

PubMed

Effective prevention of tumor metastasis would be a great contribution to the therapy of malignant tumors. Recent progress in the research of adhesion molecules has revealed that cell adhesion is an essential process in tumor metastasis. In this study, we discuss the possible involvement of adhesion molecules in various steps of tumor metastasis. PMID:8439182

Miyasaka, M; Toyama-Sorimachi, N

1993-02-01

318

Mechanisms of Adhesion in Geckos  

Microsoft Academic Search

SYNOPSIS. The extraordinary adhesive capabilities of geckos have challenged explanation for millennia, since Aristotle first recorded his observations. We have discovered many of the secrets of gecko adhesion, yet the millions of dry, adhesive setae on the toes of geckos continue to generate puzzling new questions and valuable answers. Each epidermally-derived, keratinous seta ends in hundreds of 200 nm spatular

KELLAR AUTUMN; ANNE M. PEATTIE

2002-01-01

319

Bacterial adhesion: A physicochemical approach  

Microsoft Academic Search

The adhesion of bacteria to solid surfaces was studied using a physicochemical approach. Adhesion to negatively charged polystyrene was found to be reversible and could be described quantitatively using the DLVO theory for colloidal stability, i.e., in terms of Van der Waals and electrostatic interactions. The influence of the latter was assessed by varying the electrolyte strength. Adhesion increased with

Mark C. M. van Loosdrecht; Johannes Lyklema; Willem Norde; Alexander J. B. Zehnder

1989-01-01

320

Corrugated pipe adhesive applicator apparatus  

Microsoft Academic Search

Apparatus for coating selected portions of the troughs of a corrugated pipe within an adhesive includes a support disposed within the pipe with a reservoir containing the adhesive disposed on the support. A pump, including a spout, is utilized for supplying the adhesive from the reservoir to a trough of the pipe. A rotatable applicator is supported on the support

Shirey; Ray A

1983-01-01

321

Corrugated pipe adhesive applicator apparatus  

Microsoft Academic Search

Apparatus for coating selected portions of the troughs of a corrugated pipe with an adhesive includes a support disposed within the pipe with a reservoir containing the adhesive disposed on the support. A pump, including a spout, is utilized for supplying the adhesive from the reservoir to a trough of the pipe. A rotatable applicator is supported on the support

Shirey

1983-01-01

322

Analysis of thermal conductivity in composite adhesives  

Microsoft Academic Search

Thermally conductive composite adhesives are desirable in many industrial applications, including computers, microelectronics, machinery and appliances. These composite adhesives are formed when a filler particle of high conductivity is added to a base adhesive. Typically, adhesives are poor thermal conductors. Experimentally only small improvements in the thermal properties of the composite adhesives over the base adhesives have been observed. A

Kathleen Louise Bihari

2001-01-01

323

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

324

Dynamics of Nanoparticle Adhesion  

NASA Astrophysics Data System (ADS)

We have performed molecular dynamics simulations of peeling of nanoparticles from substrate to understand the dynamics of nanoparticle adhesion. In our simulations we have calculated the potential of mean force characterizing the strength of the nanoparticle interaction with the substrate as a function of the particle-substrate separation. These simulations have shown that the detachment of the nanoparticle from substrate occurs through neck formation. The neck height decreases with increasing nanoparticle shear modulus (crosslinking density). Furthermore our simulations have established that the detachment time tR scales with the applied force as f-5. This strong force dependence is a result of the fine interplay between nanoparticle surface energy, elastic energy and its adhesion to the substrate that controls the shape of the nanoparticle.

Dobrynin, Andrey; Carrillo, Jan-Michael; Raphael, Elie

2012-02-01

325

A novel cyclin-dependent kinase inhibitor down-regulates tumor necrosis factor-? (TNF-?)-induced expression of cell adhesion molecules by inhibition of NF-?B activation in human pulmonary epithelial cells  

Microsoft Academic Search

BAI (a novel cyclin-dependent kinase (CDK) inhibitor, 2-[1,1?-biphenyl]-4-yl-N-[5-(1,1-dioxo-1?6-isothiazolidin-2-yl)-1H-indazol-3-yl] acetamide) is known to have anti-proliferative activity, but the mechanism responsible for it remains unclear. We here investigated the functional effect of BAI on airway inflammation and its action mechanism. BAI down-regulated the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in human lung epithelial A549 cells stimulated

Jung Hwa Oh; Eun Jung Park; Jong-Wook Park; Jinho Lee; Sang Han Lee; Taeg Kyu Kwon

2010-01-01

326

Adhesion of Nanoparticles  

Microsoft Academic Search

We have developed a new model of nanoparticle adhesion which explicitly takes into account the change in the nanoparticle surface energy. Using combination of the molecular dynamics simulations and theoretical calculations we have showed that the deformation of the adsorbed nanoparticles is a function of the dimensionless parameter betagamma( GR )-2\\/3W-1\\/3, where G is the particle shear modulus, R is

Jan-Michael Carrillo; Elie Raphael; Andrey Dobrynin

2011-01-01

327

Engineering Cell Adhesion  

Microsoft Academic Search

\\u000a Cells exist within a complex and ever-changing environment, which includes soluble molecules such as growth factors, an extracellular\\u000a matrix that includes adhesive proteins and carbohydrates, and other neighboring cells. They actively sense and respond to\\u000a changes in this environment, existing in a state of physiological equilibrium with it. Thus, it has been said, “. . . the\\u000a unit of function

Kiran Bhadriraju; Wendy F. Liu; Darren S. Gray; Christopher S. Chen

328

[Fulminant adhesive arachnoiditis].  

PubMed

Adhesive arachnoiditis is a rare disease with insidious course. It causes damage of the spinal cord and nerve roots. The causes of adhesive arachnoiditis include earlier traumatic injury of the spinal cord, surgery, intrathecal administration of therapeutic substances (e.g. anaesthetics, chemotherapy) or contrast media, bleeding, and inflammation. It can also be idiopathic or iatrogenic. We present the case of a 42-year-old patient with fulminant adhesive arachnoiditis which was provoked by spinal surgery and caused severe neurological disability with profound, progressive, flaccid paraparesis and bladder dysfunction. The electromyography (EMG) showed serious damage of nerves of both lower limbs at the level of motor roots L2-S2 and damage of the motor neuron at the level of Th11-Th12 on the right side. Magnetic resonance imaging of the lumbosacral and thoracic part of the spinal cord demonstrated cystic liquid spaces in the lumen of the dural sac in the bottom part of the cervical spine and at the Th2-Th10 level, modelling the lateral and anterior surface of the cord. Because of the vast lesions, surgery could not be performed. Conservative treatment and rehabilitation brought only a small clinical improvement. PMID:23023442

Tomczykiewicz, Kazimierz; St?pie?, Adam; Staszewski, Jacek; Sadowska, Marta; Bogus?awska-Walecka, Romana

329

Inflammatory factors in major and macular branch retinal vein occlusion.  

PubMed

Concentrations of inflammatory factors were measured in 40 patients with macular edema due to major branch retinal vein occlusion (BRVO) or macular BRVO who were treated by pars plana vitrectomy. Vitreous fluid levels of vascular endothelial growth factor (VEGF), soluble intercellular adhesion molecule-1 (sICAM-1), and pigment epithelium-derived factor (PEDF) were determined. Visual acuity and central macular thickness were significantly improved at 6 months in both groups. Vitreous fluid levels of VEGF and sICAM-1 were higher in the major BRVO group than the macular BRVO group, while the PEDF level was lower in the major group than the macular group. The mean visual acuity and central macular thickness at 6 months were not significantly different between the macular and major groups. In conclusion, patients with major BRVO had higher vitreous levels of inflammatory factors and lower vitreous levels of anti-inflammatory PEDF. Accordingly, regulating inflammatory factors might be more important in major BRVO than macular BRVO. PMID:22269605

Noma, Hidetaka; Funatsu, Hideharu; Mimura, Tatsuya; Eguchi, Shuichiro; Shimada, Katsunori

2012-01-20

330

High-mobility group box-1 induces decreased brain-derived neurotrophic factor-mediated neuroprotection in the diabetic retina.  

PubMed

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. PMID:23766563

Abu El-Asrar, Ahmed M; Nawaz, Mohd Imtiaz; Siddiquei, Mohammad Mairaj; Al-Kharashi, Abdullah S; Kangave, Dustan; Mohammad, Ghulam

2013-05-20

331

Femoral artery remodeling after aerobic exercise training without weight loss in women  

PubMed Central

Background It is currently unclear whether reductions in adiposity mediate the improvements in vascular health that occur with aerobic exercise. The purpose of this longitudinal study of 13 healthy women (33 ± 4 years old) was to determine whether 14 weeks of aerobic exercise would alter functional measures of vascular health, namely resting aortic pulse wave velocity (aPWV, an index of arterial stiffness), femoral artery diameter (DFA), and femoral artery blood flow (BFFA) independent of changes in adiposity. Methods Aerobic fitness was assessed as VO2peak normalized to fat-free mass, and adiposity (percent body fat) was determined by dual energy x-ray absorptiometry. Serum concentrations of proteins associated with risk for cardiovascular disease, including C-reactive protein (CRP), soluble intercellular adhesion molecule-1 (sICAM-1), and leptin, were also measured. Subjects cycled for 50 minutes, 3 times per week. Results Aerobic fitness normalized to fat-free mass increased 6% (P = 0.03) whereas adiposity did not change. Resting DFA increased 12% (P < 0.001) and resting shear rate decreased 28% (P = 0.007). Aortic PWV, and serum sICAM-1, CRP and leptin did not change with training. Conclusion Significant reductions in adiposity were not necessary for aerobic exercise training to bring about improvements in aerobic fitness and arterial remodeling. Peripheral arterial remodeling occurred without changes in central arterial stiffness or markers of inflammation.

Sabatier, Manning J; Schwark, Earl H; Lewis, Richard; Sloan, Gloria; Cannon, Joseph; McCully, Kevin

2008-01-01

332

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

333

Dynamic adhesions and MARCKS in melanoma cells  

PubMed Central

Summary Cell motility necessitates the rapid formation and disassembly of cell adhesions. We have studied adhesions in a highly motile melanoma cell line using various biochemical approaches and microscopic techniques to image close adhesions. We report that WM-1617 melanoma cells contain at least two types of close adhesion: classic focal adhesions and more extensive, irregularly shaped adhesions that tend to occur along lamellipodial edges. In contrast to focal adhesions, these latter adhesions are highly dynamic and can be disassembled rapidly via protein kinase C (PKC) activation (e.g. by eicosanoid) and MARCKS phosphorylation. MARCKS overexpression, however, greatly increases the area of close adhesions and renders them largely refractory to PKC stimulation. This indicates that nonphosphorylated MARCKS is an adhesion stabilizer. Unlike focal adhesions, the dynamic adhesions contain ?3 integrin and MARCKS, but they do not contain the focal adhesion marker vinculin. Overall, these results begin to define the molecular and functional properties of dynamic close adhesions involved in cell motility.

Estrada-Bernal, Adriana; Gatlin, Jesse C.; Sunpaweravong, Somkiat; Pfenninger, Karl H.

2009-01-01

334

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

335

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

336

Circulating IgSF proteins inhibit adhesion of antibody targeted microspheres to endothelial inflammatory ligands.  

PubMed

Proposed methods for detecting circulatory system disease include targeting ultrasound contrast agents to inflammatory markers on vascular endothelial cells. For antibody-based therapies, soluble forms of the targeted adhesion proteins of the immunoglobulin superfamily (IgSF) reduce adhesion yet were left unaccounted in prior reports. Microspheres labeled simply with a maximum level of antibodies can reduce the diagnostic sensitivity by adhering to proteins expressed normally at a low level, while sparsely coated particles may be rendered ineffective by circulating soluble forms of the targeted proteins. A new microdevice technique is applied to simultaneously measure the adhesion profile to a series of IgSF-protein-coated surfaces. In this investigation, we quantify the in vitro binding characteristics of 5-microm microspheres to oriented intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) protein-coated surfaces in the presence of human serum at physiological concentrations. Defined regions of a slide were coated with recombinant chimeric Fc-human ICAM-1 and VCAM-1 in variable ratios but constant total concentration. Monoclonal human anti-ICAM-1 or anti-VCAM-1 antibodies in competition with non-binding mouse anti-rabbit antibodies coat the microsphere surface at a constant surface density with variable yet controlled surface activities. Using multiple slide surface IgSF protein and microsphere antibody concentrations, an adhesion profile was developed for the microspheres with and without IgSF proteins from human serum, which demonstrated that exposure to serum reduced microsphere binding, on average, more than 50% compared to the no-serum condition.. The serum effects were limited to antibodies on the microsphere, since binding inhibition was reversed after rinsing serum from the system and fresh antibody-coated microspheres were introduced. This analysis quantifies the binding effects of soluble IgSF proteins from human serum on antibody-based targeted ultrasound detection and drug delivery methods. PMID:19140030

Kerby, Matthew B; Urban, Jane C; Mouallem, Lea; Tripathi, Anubhav

2009-01-13

337

Efecto de la ingesta de una sobrecarga de glucosa sobre los marcadores séricos de adhesión en mujeres obesas  

Microsoft Academic Search

Background and objectiveObesity is associated with endothelial dysfunction and increased inflammation. The expression of adhesion molecules may be influenced by a high glucose load. The aim of the present study was to evaluate serum sICAM-1, sVCAM-1 and sE-selectin concentrations in obese women, and to evaluate the role of high-glucose load on postload circulating levels of sICAM-1, sVCAM-1 and sE-selectin in

María Matilde Ramírez Alvarado; Maria Isabel García de Seijo; Evelyn Bahri Hernández; Tibisay Pelayo Jordán

2009-01-01

338

Adhesion of Coagulase-Negative Staphylococci onto Biomaterials.  

National Technical Information Service (NTIS)

Contents: In vitro bacterial adhesion onto solid surfaces; Physico-chemical aspects of bacterial adhesion; Experimental models for bacterial adhesion, studies, Bacterial adhesion structures, properties and bacterial adhesion, bacterial adhesion related to...

A. H. Hogt

1985-01-01

339

Simultaneous height and adhesion imaging of antibody-antigen interactions by atomic force microscopy.  

PubMed Central

Specific molecular recognition events, detected by atomic force microscopy (AFM), so far lack the detailed topographical information that is usually observed in AFM. We have modified our AFM such that, in combination with a recently developed method to measure antibody-antigen recognition on the single molecular level (Hinterdorfer, P., W. Baumgartner, H. J. Gruber, K. Schilcher, and H. Schindler, Proc. Natl. Acad. Sci. USA 93:3477-3481 (1996)), it allows imaging of a submonolayer of intercellular adhesion molecule-1 (ICAM-1) in adhesion mode. We demonstrate that for the first time the resolution of the topographical image in adhesion mode is only limited by tip convolution and thus comparable to tapping mode images. This is demonstrated by imaging of individual ICAM-1 antigens in both the tapping mode and the adhesion mode. The contrast in the adhesion image that was measured simultaneously with the topography is caused by recognition between individual antibody-antigen pairs. By comparing the high-resolution height image with the adhesion image, it is possible to show that specific molecular recognition is highly correlated with topography. The stability of the improved microscope enabled imaging with forces as low as 100 pN and ultrafast scan speed of 22 force curves per second. The analysis of force curves showed that reproducible unbinding events on subsequent scan lines could be measured.

Willemsen, O H; Snel, M M; van der Werf, K O; de Grooth, B G; Greve, J; Hinterdorfer, P; Gruber, H J; Schindler, H; van Kooyk, Y; Figdor, C G

1998-01-01

340

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

341

Cholesterol induces apoptosis-associated loss of the activated leukocyte cell adhesion molecule (ALCAM) in human monocytes.  

PubMed

The activated leukocyte cell adhesion molecule (ALCAM/CD166) is associated with cell migration and leukocyte invasion into the vessel wall. This study investigates the impact of cholesterol loading on the expression of ALCAM, as compared with P-selectin glycoprotein ligand-1 (PSGL-1), vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) in monocytic U937 cells and human primary monocytes. Cells were enriched with cholesterol by incubation with a cyclodextrin-cholesterol complex. Expression of adhesion molecules and apoptosis was determined by flow cytometry. Migration was quantified by chemotaxis toward serum. Incubation with cholesterol (10-100 ?g/ml) for 16 h caused a concentration-dependent increase in apoptosis. Enhanced apoptosis was associated with reduction of ALCAM by >70%. While PSGL-1 was affected similarly, expression of VCAM-1 was markedly increased by cholesterol and ICAM-1 levels were not regulated. The nonselective caspase/apoptosis inhibitor Q-VD-OPh partially prevented cholesterol-modulated alteration of adhesion molecule expression. Migration of cholesterol-rich monocytic cells toward serum was greatly reduced. This effect was partially restored by Q-VD-OPh and was dependent on ALCAM as shown by ALCAM-neutralizing antibodies. In conclusion, cholesterol-induced apoptosis in monocytes is accompanied by reduced expression of ALCAM and attenuated monocyte migration. This may restrain monocytes at cholesterol-rich sites and thereby expedite vascular lesion formation. PMID:21440089

Rauch, Stefan J; Rosenkranz, Anke C; Böhm, Andreas; Meyer-Kirchrath, Jutta; Hohlfeld, Thomas; Schrör, Karsten; Rauch, Bernhard H

2011-03-31

342

Effects of monoclonal antibodies to adhesion molecules on eosinophilic myocarditis in Toxocara canis-infected CBA/J mice  

PubMed Central

Eosinophilic myocarditis followed by fibrosis of the cardiac muscle was observed in addition to peripheral blood eosinophilia in CBA/J mice infected with Toxocara canis. The infected mice were used as an experimental model of eosinophilic endomyocarditis associated with hypereosinophilic syndrome. Effects of in vivo treatment with MoAbs to adhesion molecules on eosinophilic myocarditis were examined using this experimental model. Expressions of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) on endothelial cells of capillaries in myocardium were increased 1 and 2 weeks after infection. Infiltration of very late antigen (VLA)-4+ and/or CD11a+ cells into the cardiac muscles was also observed 1 and 2 weeks after infection. Infiltration of eosinophils into the heart was significantly suppressed by anti-CD18 MoAb and anti-VLA-4 MoAb, and focal fibrosis of the cardiac muscle was also significantly suppressed by combined administration of anti-CD18 and anti-ICAM-1 MoAbs. These results indicate that adhesion molecules may play important roles in eosinophilic myocarditis, and that blockade of interaction between adhesion molecules and their ligands may help to control it.

Hokibara, S; Takamoto, M; Isobe, M; Sugane, K

1998-01-01

343

Nitric oxide decreases cytokine-induced endothelial activation. Nitric oxide selectively reduces endothelial expression of adhesion molecules and proinflammatory cytokines.  

PubMed

To test the hypothesis that nitric oxide (NO) limits endothelial activation, we treated cytokine-stimulated human saphenous vein endothelial cells with several NO donors and assessed their effects on the inducible expression of vascular cell adhesion molecule-1 (VCAM-1). In a concentration-dependent manner, NO inhibited interleukin (IL)-1 alpha-stimulated VCAM-1 expression by 35-55% as determined by cell surface enzyme immunoassays and flow cytometry. This inhibition was paralleled by reduced monocyte adhesion to endothelial monolayers in nonstatic assays, was unaffected by cGMP analogues, and was quantitatively similar after stimulation by either IL-1 alpha, IL-1 beta, IL-4, tumor necrosis factor (TNF alpha), or bacterial lipopolysaccharide. NO also decreased the endothelial expression of other leukocyte adhesion molecules (E-selectin and to a lesser extent, intercellular adhesion molecule-1) and secretable cytokines (IL-6 and IL-8). Inhibition of endogenous NO production by L-N-monomethyl-arginine also induced the expression of VCAM-1, but did not augment cytokine-induced VCAM-1 expression. Nuclear run-on assays, transfection studies using various VCAM-1 promoter reporter gene constructs, and electrophoretic mobility shift assays indicated that NO represses VCAM-1 gene transcription, in part, by inhibiting NF-kappa B. We propose that NO's ability to limit endothelial activation and inhibit monocyte adhesion may contribute to some of its antiatherogenic and antiinflammatory properties within the vessel wall. PMID:7542286

De Caterina, R; Libby, P; Peng, H B; Thannickal, V J; Rajavashisth, T B; Gimbrone, M A; Shin, W S; Liao, J K

1995-07-01

344

Ginsenoside Rg3 inhibits tumor necrosis factor-alpha-induced expression of cell adhesion molecules in human endothelial cells.  

PubMed

Ginsenoside Rg3 (Rg3), one of the most effective ginseng saponins, has anti-inflammatory and anti-cancer effects. This study examined the effects of Rg3 on cytokine-induced expression of adhesion molecules, which is a key early event in atherogenesis. Rg3 treatment inhibited tumor necrosis factor-alpha (TNF-alpha)-induced protein and mRNA expression of two cell adhesion molecules, vascular cell adhesion molecule-1 (VCAM-1) and intercellular cell adhesion molecule-1 (ICAM-1) in ECV 304 human endothelial cells. In addition, expression of two pro-inflammatory cytokines, TNF-alpha and interleukin-1beta (IL-1beta), was suppressed by Rg3. Reporter gene analyses revealed that minimal reporter activities of nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1) were blocked by Rg3 in a concentration-dependent manner. Taken together, these results indicate that Rg3 may have anti-inflammatory and anti-atherosclerotic activities in the vasculature, which is mediated partly by down-regulation of the expression of cell adhesion molecules and proinflammatory cytokines in endothelial cells. PMID:21038849

Hien, Tran Thi; Kim, Nak Doo; Kim, Hyung Sik; Kang, Keon Wook

2010-09-01

345

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

346

[Intrauterine adhesions--Asherman's syndrome].  

PubMed

Intrauterine adhesions known as Asherman's syndrome evolve after trauma to the basal layer of the endometrium usually secondary to curettage of a recently pregnant uterus. The lesions range from minor to severe cohesive adhesions that affect menstrual function and fertility. Operative hysteroscopy is the mainstay of diagnosis, classification and treatment of the intrauterine adhesions. Significantly obliterated cavity may require multiple hysteroscopic adhesiolysis to achieve a satisfactory anatomical and functional result. Operative hysteroscopy for selective curettage of residual trophoblastic tissue instead of nonselective conventional curettage may prevent intrauterine adhesions. PMID:21171473

Heinonen, Pentti K

2010-01-01

347

Intercellular adhesion molecule-I (ICAM-I, CD54) deficiency segregates the unique pathophysiological requirements for generating idiopathic pneumonia syndrome (IPS) versus graft-versus-host disease following allogeneic murine bone marrow transplantation  

Microsoft Academic Search

Following allogeneic bone marrow transplantation (alloBMT), idiopathic pneumonia syndrome (IPS) and graft-versus-host disease (GVHD) caused by donor cell alloreactivity remain major obstacles to a successful outcome. Intercellular adhesion molecule-1 (ICAM-1) is an adhesion molecule that is involved in regulating lymphohematopoietic cell migration and facilitating T-cell responses. To determine whether ICAM-1 expression in the host would affect IPS or GVHD tissue

Angela Panoskaltsis-Mortari; John R Hermanson; Imad Y Haddad; O. Douglas Wangensteen; Bruce R Blazar

2001-01-01

348

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

349

Differential adhesion in model systems.  

PubMed

During embryonic development, cells or groups of cells migrate from their locations of origin to assume their correct anatomical positions. Intercellular adhesion plays an active and instructive role in orchestrating this process. Precisely how adhesion provides spatial positioning information is a subject of intense interest. In the 1960s, Steinberg proposed the differential adhesion hypothesis (DAH) to explain how differences in the intensity of cell adhesion could give rise to predictable spatial interactions between different cell types. The DAH is grounded in the same set of physical principles governing the interaction of immiscible fluids and thus provides a rigorous conceptual framework connecting the chemistry of cell adhesion to the physics underlying cell and tissue segregation. Testing the DAH required the development of methods to measure intercellular cohesion and of assays to accurately assess relative spatial position between cells. The DAH has been experimentally verified and computationally simulated. Moreover, evidence concerning the role of differential adhesion in a number of morphodynamic events is accumulating. It is clear that differential adhesion is a major driving force in various aspects of embryonic development, but recent studies have also advanced the concept that other factors, such as cortical tension and elasticity, may also be involved in fine tuning, or even driving the process. It is likely that an interplay between adhesion and these other factors co-operate to generate the forces required for tissue self-organization. PMID:24014451

Foty, Ramsey A; Steinberg, Malcolm S

2013-01-30

350

Serum concentrations of soluble adhesion molecules in patients with colorectal cancer.  

PubMed Central

The concentrations of the soluble adhesion molecules E-cadherin, E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) were investigated in 48 patients with colorectal cancer before treatment, and their relation to clinical, histological and routine laboratory parameters was examined. Data were collected on tumour stage at presentation, presence and sites of metastatic disease, tumour pathology and results of routine laboratory tests. Serum concentrations of ICAM-1 and VCAM-1 were significantly elevated in the patients with colorectal cancer in comparison with a group of healthy subjects (P < 0.00001). Levels of circulating ICAM-1 and VCAM-1 were increased both in patients with local and those with metastatic disease. Although elevated in some patients soluble E-cadherin and E-selectin concentrations were not significantly elevated compared with the control group (P = 0.71 and P = 0.052 respectively). The levels of circulating ICAM-1 were significantly correlated with those of VCAM-1 and E-selectin. A correlation was also found between the serum concentrations of E-selectin and ICAM-1 and alkaline phosphatase, total white cell count and platelet count. VCAM-1 was positively correlated with age and negatively with degree of tumour differentiation and haemoglobin concentration. The biological implications and possible clinical relevance of these findings are discussed.

Velikova, G.; Banks, R. E.; Gearing, A.; Hemingway, I.; Forbes, M. A.; Preston, S. R.; Hall, N. R.; Jones, M.; Wyatt, J.; Miller, K.; Ward, U.; Al-Maskatti, J.; Singh, S. M.; Finan, P. J.; Ambrose, N. S.; Primrose, J. N.; Selby, P. J.

1998-01-01

351

Biological adhesives and fastening devices  

NASA Astrophysics Data System (ADS)

Sea creatures are a leading source to some of the more interesting discoveries in adhesives. Because sea water naturally breaks down even the strongest conventional adhesive, an alternative is important that could be used in repairing or fabricating anything that might have regular contact with moisture such as: Repairing broken and shattered bones, developing a surgical adhesive, use in the dental work, repairing and building ships, and manufacturing plywood. Some of nature's prototypes include the common mussel, limpet, some bacteria and abalone. As we learn more about these adhesives we are also developing non adhesive fasteners, such as mimicked after studying the octopus, burdock burrs (i.e. Velcro®) and the gecko.

Wolpert, H. D.

2012-03-01

352

Corrugated pipe adhesive applicator apparatus  

DOEpatents

Apparatus for coating selected portions of the troughs of a corrugated pipe within an adhesive includes a support disposed within the pipe with a reservoir containing the adhesive disposed on the support. A pump, including a spout, is utilized for supplying the adhesive from the reservoir to a trough of the pipe. A rotatable applicator is supported on the support and contacts the trough of the pipe. The applicator itself is sized so as to fit within the trough, and contacts the adhesive in the trough and spreads the adhesive in the trough upon rotation. A trough shield, supported by the support and disposed in the path of rotation of the applicator, is utilized to prevent the applicator from contacting selected portions of the trough. A locator head is also disposed on the support and provides a way for aligning the spout, the applicator, and the trough shield with the trough.

Shirey, Ray A. (North Grafton, MA)

1983-06-14

353

Corrugated pipe adhesive applicator apparatus  

DOEpatents

Apparatus for coating selected portions of the troughs of a corrugated pipe with an adhesive includes a support disposed within the pipe with a reservoir containing the adhesive disposed on the support. A pump, including a spout, is utilized for supplying the adhesive from the reservoir to a trough of the pipe. A rotatable applicator is supported on the support and contacts the trough of the pipe. The applicator itself is sized so as to fit within the trough, and contacts the adhesive in the trough and spreads the adhesive in the trough upon rotation. A trough shield, supported by the support and disposed in the path of rotation of the applicator, is utilized to prevent the applicator from contacting selected portions of the trough. A locator head is also disposed on the support and provides a way for aligning the spout, the applicator, and the trough shield with the trough. 4 figs.

Shirey, R.A.

1983-06-14

354

Early Vascular Alterations in SLE and RA Patients--A Step towards Understanding the Associated Cardiovascular Risk  

PubMed Central

Accelerated atherosclerosis represents a major problem in both systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) patients, and endothelial damage is a key feature of atherogenesis. We aimed to assess early endothelial changes in SLE and RA female patients (127 SLE and 107 RA) without previous CV events. Biomarkers of endothelial cell activation (intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (sVCAM-1), thrombomodulin (TM), and tissue factor (TF)) were measured and endothelial function was assessed using peripheral artery tonometry. Reactive hyperemia index (RHI), an indicator of microvascular reactivity, and augmentation index (AIx), a measure of arterial stiffness, were obtained. In addition, traditional CV risk factors, disease activity and medication were determined. Women with SLE displayed higher sICAM-1 and TM and lower TF levels than women with RA (p?=?0.001, p<0.001 and p<0.001, respectively). These differences remained significant after controlling for CV risk factors and medication. Serum levels of vascular biomarkers were increased in active disease and a moderate correlation was observed between sVCAM-1 levels and lupus disease activity (rho?=?0.246) and between TF levels and RA disease activity (rho?=?0.301). Although RHI was similar across the groups, AIx was higher in lupus as compared to RA (p?=?0.04). Also in active SLE, a trend towards poorer vasodilation was observed (p?=?0.06). In conclusion, women with SLE and RA present with distinct patterns of endothelial cell activation biomarkers not explained by differences in traditional CV risk factors. Early vascular alterations are more pronounced in SLE which is in line with the higher CV risk of these patients.

Santos, Maria Jose; Carmona-Fernandes, Diana; Canhao, Helena; Canas da Silva, Jose; Fonseca, Joao Eurico; Gil, Victor

2012-01-01

355

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

356

Effect of prior exercise on postprandial lipemia and markers of inflammation and endothelial activation in normal weight and overweight adolescent boys.  

PubMed

Postprandial lipemia (PPL) is associated with impaired endothelial function and inflammation. Acute exercise reduces PPL in adults. This investigation examined the effect of an acute bout of exercise on postprandial changes in triglycerides (TG), glucose, insulin, inflammation [white blood cell count (WBC), interleukin-6 (IL-6) tumor necrosis factor-alpha, C-reactive protein (CRP)] and endothelial activation [soluble intercellular adhesion molecule-1 (sICAM-1), vascular adhesion molecule-1 (sVCAM-1)] following a high-fat meal in adolescents. Ten normal weight (NW) (BMI, 20.9 +/- 1.7 kg m(-2); 15.6 +/- 0.7 years) and eight overweight (OW) (BMI, 28.3 +/- 3.6 kg m(-2); 15.9 +/- 0.4 years) adolescent boys underwent two 6-h oral fat tolerance tests (OFTT) separated by 7-10 days. On the evening prior to each OFTT, subjects either rested or completed a treadmill exercise bout (65% V(O)(2max); 600 kcal expended). Exercise reduced (P < 0.01) the postprandial TG area under the curve by approximately 20% in the NW and OW groups. The postprandial glucose and insulin response did not differ between the control and exercise trials or between the NW and OW groups. Circulating leukocytes and plasma IL-6 levels increased (P < 0.01) in the NW and OW groups 6 h following the OFTT in both experimental conditions. There were no changes in CRP, sVCAM-1 or sICAM-1 following the OFTT and there were no differences between experimental condition or NW and OW groups. In conclusion, a moderate exercise bout prior to a high-fat meal effectively reduces postprandial TG concentrations to a similar degree in both NW and OW adolescents, but does not reduce the concomitant postprandial increase in WBC or IL-6. PMID:19430945

MacEneaney, Owen J; Harrison, Michael; O'Gorman, Donal J; Pankratieva, Elena V; O'Connor, Paul L; Moyna, Niall M

2009-05-10

357

Zofenopril inhibits the expression of adhesion molecules on endothelial cells by reducing reactive oxygen species.  

PubMed

Hypertension and coronary artery disease are intimately connected. The migration of circulating monocytes into the subendothelial occurs through the expression of some adhesion molecules on endothelial cells. The nuclear factor (NF)-kappaB, a redox-sensitive element, plays a key role in adhesion molecule gene induction. In this study we have compared the effects of two different angiotensin converting enzyme (ACE) inhibitors, one possessing an active sulfhydryl group (zofenopril) and one lacking this group (enalapril) on the cellular redox state (monitored by measuring intracellular reactive oxygen species and thiol status), expression of adhesion molecules, and activation of NF-kappaB in human umbilical vein endothelial cells (HUVECs). Zofenoprilat, the active form of zofenopril, significantly and dose dependently reduced the intracellular reactive oxygen species (ROS) and superoxide formation induced by oxidized low-density lipoprotein (ox-LDL) (P <.001) and tumor necrosis factor-alpha (TNF-alpha) (P <.001). Enalaprilat, the active form of enalapril, was ineffective. Zofenoprilat but not enalaprilat also decreased the consumption of the intracellular GSH induced by ox-LDL (P <.01) and TNF-alpha (P <.01). Although zofenoprilat significantly and dose dependently reduced the expression of vascular cell adhesion molecule-1 (VCAM-1), intercellular cell adhesion molecule-1 (ICAM-1), and E-selectin induced by ox-LDL (P <.01) and TNF-alpha (P <.01) on HUVECs, enalaprilat did not. Ox-LDL and TNF-alpha increased the activation of NF-kappaB and the preincubation of HUVECs with zofenoprilat, but not with enalaprilat, dose dependently reduced its activation (P <.001). The conclusion is that the sulfhydryl (SH)-containing ACE inhibitors may be useful in inhibiting foam cell formation and thus slow the development of atherosclerosis. PMID:12372676

Cominacini, Luciano; Pasini, Anna; Garbin, Ulisse; Evangelista, Stefano; Crea, Attilio E G; Tagliacozzi, Debora; Nava, Cristina; Davoli, Anna; LoCascio, Vincenzo

2002-10-01

358

Soluble adhesion molecules and cytokines in children affected by recurrent infections of the upper respiratory tract.  

PubMed

The objective of this study was to compare plasma levels of soluble adhesion molecules and Th1-Th2 type cytokines in 44 children with frequently recurrent respiratory infections (FRRI) of upper airways, defined as having nine or more episodes per year, and in 34 children without recurrence; all subjects were followed-up for 12 mo. The viral etiology was determined by cultures from nasal, pharyngeal, and ear secretions, using PCR and immunofluorescence. Plasma levels of five soluble adhesion molecules (E-selectin, P-selectin, L-selectin, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1) and interferon (IFN)-gamma, IL-12, IL-4, and IL-10 were measured in patients and in 15 healthy controls using sandwich ELISA. During acute phase, all patients showed significant increase in plasma levels of soluble adhesion molecules; during the follow-up, the levels were greater in children with FRRI. A difference of cytokine profile was demonstrated between the patients with and without FRRI: an increased IL-4 and IL-10 release with decreased levels of IFN-gamma and IL-12 suggested a skewing into Th2-type response, in patients with FRRI. This pattern persisted during the follow-up. In patients without recurrence, an increased IFN-gamma and IL-12 release, together with decreased levels of IL-4 and IL-10, showed a skewing into Th1-type responses; in the follow-up these cytokines reached normal values. In conclusion, the abnormal levels of all examined parameters in children with FRRI may reflect the persistence of an inflammatory microenvironment in the airways and an activation of the immune system that may contribute to the frequently recurrence of the respiratory disease. PMID:14711887

Malaponte, Grazia; Bevelacqua, Valentina; Li Volti, Giovanni; Petrina, Marcello; Nicotra, Giusy; Sapuppo, Valentina; Li Volti, Salvatore; Travali, Salvatore; Mazzarino, Maria Clorinda

2004-01-07

359

Kindlins in FERM adhesion.  

PubMed

The Kindlin family of intracellular proteins has recently emerged as key regulators of cellular functions and cell-matrix interactions. The 3 members of this family, Kindlin-1, -2, and -3, perform an essential role in activation of integrin adhesion receptors, and expression of at least 1 Kindlin paralog is required to enable integrin activation in physiologically relevant settings. In humans, deficiencies in Kindlin-3 lead to a number of abnormalities affecting hemostasis, the immune system, and bone function, whereas the lack of Kindlin-1 causes profound skin defects. The importance of Kindlins is underscored by the results of animal knockout studies, which clearly show the indispensable and nonredundant functions of all 3 Kindlins in development and normal physiology. This review discusses recent progress in the studies of Kindlin protein family, emphasizing newly identified functions and potential mechanisms underlying differential activities of the family members. PMID:20228270

Malinin, Nikolay L; Plow, Edward F; Byzova, Tatiana V

2010-03-12

360

Kindlins in FERM adhesion  

PubMed Central

The Kindlin family of intracellular proteins has recently emerged as key regulators of cellular functions and cell-matrix interactions. The 3 members of this family, Kindlin-1, -2, and -3, perform an essential role in activation of integrin adhesion receptors, and expression of at least 1 Kindlin paralog is required to enable integrin activation in physiologically relevant settings. In humans, deficiencies in Kindlin-3 lead to a number of abnormalities affecting hemostasis, the immune system, and bone function, whereas the lack of Kindlin-1 causes profound skin defects. The importance of Kindlins is underscored by the results of animal knockout studies, which clearly show the indispensable and nonredundant functions of all 3 Kindlins in development and normal physiology. This review discusses recent progress in the studies of Kindlin protein family, emphasizing newly identified functions and potential mechanisms underlying differential activities of the family members.

Malinin, Nikolay L.; Plow, Edward F.

2010-01-01

361

New technology for wood adhesives and coatings  

Treesearch

Treesearch Home ... Keywords: Glue, adhesion, adhesives, testing, coatings, research projects, technological innovations, microscopy, spectroscopy, gluing, wood chemistry, wood bonding, bond strength, bonding, durability, gluing, failure,  ...

362

MORPHEUS' MOLECULE1 Is Required to Prevent Aberrant RNA Transcriptional Read-Through in Arabidopsis1[C][W][OA  

PubMed Central

Several pathways function to remove aberrant mRNA in eukaryotic cells; however, the exact mechanisms underlying the restriction of aberrant mRNA transcription are poorly understood. In this study, we found that MORPHEUS’ MOLECULE1 (MOM1) is a key component of this regulatory machinery. The Arabidopsis (Arabidopsis thaliana) mom1-44 mutation was identified by luciferase imaging in transgenic plants harboring a cauliflower mosaic virus 35S promoter-LUCIFERASE transgene lacking the 3?-untranslated region. In the mom1-44 mutant, transcriptional read-though occurred in genes with an aberrant RNA structure. Analysis of an RNA-dependent RNA polymerase2 mom1 double mutant revealed that the RNA-directed DNA methylation pathway is not involved in this regulatory process. Moreover, the prevention of aberrant mRNA transcriptional read-through by MOM1 is gene locus and transgene copy number independent.

Zhou, Yue; Zhang, Jun; Lin, Huixin; Guo, Guangqin; Guo, Yan

2010-01-01

363

Inhibition of tumor necrosis factor-{alpha}-induced expression of adhesion molecules in human endothelial cells by the saponins derived from roots of Platycodon grandiflorum  

SciTech Connect

Adhesion molecules play an important role in the development of atherogenesis and are produced by endothelial cells after being stimulated with various inflammatory cytokines. This study examined the effect of saponins that were isolated from the roots of Platycodon grandiflorum A. DC (Campanulaceae), Changkil saponins (CKS), on the cytokine-induced monocyte/human endothelial cell interaction, which is a crucial early event in atherogenesis. CKS significantly inhibited the TNF{alpha}-induced increase in monocyte adhesion to endothelial cells as well as decreased the protein and mRNA expression levels of vascular adhesion molecule-1 and intercellular cell adhesion molecule-1 on endothelial cells. Furthermore, CKS significantly inhibited the TNF{alpha}-induced production of intracellular reactive oxygen species (ROS) and activation of NF-{kappa}B by preventing I{kappa}B degradation and inhibiting I{kappa}B kinase activity. Overall, CKS has anti-atherosclerotic and anti-inflammatory activity, which is least in part the result of it reducing the cytokine-induced endothelial adhesion to monocytes by inhibiting intracellular ROS production, NF-{kappa}B activation, and cell adhesion molecule expression in endothelial cells.

Kim, Ji Young [Department of Pharmacy, College of Pharmacy, Research Center for Proteineous Materials, Chosun University, Kwangju (Korea, Republic of); Kim, Dong Hee [Department of Pathology, College of Oriental Medicine, Daejeon University, Daejeon (Korea, Republic of); Kim, Hyung Gyun [Department of Pharmacy, College of Pharmacy, Research Center for Proteineous Materials, Chosun University, Kwangju (Korea, Republic of); Song, Gyu-Yong [Department of Pharmacy, College of Pharmacy, Chungnam National University, Taejon (Korea, Republic of); Chung, Young Chul [Division of Food Science, Chinju International University, Chinju (Korea, Republic of); Roh, Seong Hwan [Jangsaeng Doraji Research Institute of Biotechnology, Jangsaeng Doraji Co., Ltd., Chinju (Korea, Republic of); Jeong, Hye Gwang [Department of Pharmacy, College of Pharmacy, Research Center for Proteineous Materials, Chosun University, Kwangju (Korea, Republic of)]. E-mail: hgjeong@chosun.ac.kr

2006-01-15

364

Dynamics of nanoparticle adhesion  

NASA Astrophysics Data System (ADS)

We performed molecular dynamics simulations and theoretical analysis of nanoparticle pulling off from adhesive substrates. Our theoretical model of nanoparticle detachment is based on the Kramers' solution of the stochastic barrier crossing in effective one-dimensional potential well. The activation energy, ?E, for nanoparticle detachment first decreases linearly with increasing the magnitude of the applied force, f, then it follows a power law ?E ~ (f* - f)3/2 as magnitude of the pulling force f approaches a critical detachment force value, f*. These two different regimes in activation energy dependence on magnitude of the applied force are confirmed by analyzing nanoparticle detachment in effective one-dimensional potential obtained by weighted histogram analysis method. Simulations show that detachment of nanoparticle proceeds through neck formation such that magnitude of the activation energy is determined by balancing surface energy of the neck connecting particle to a substrate with elastic energy of nanoparticle deformation. In this regime the activation energy at zero applied force, ?E0, for nanoparticle with radius, Rp, shear modulus, G, surface energy, ?p, and work of adhesion, W, is a universal function of the dimensionless parameter ? ~?pW-2/3(GRp)-1/3. Simulation data are described by a scaling function ?E0~?p5/2Rp1/2G-3/2?-3.75. Molecular dynamics simulations of nanoparticle detachment show that the Kramers' approach fails in the vicinity of the critical detachment force f* where activation energy barrier becomes smaller than the thermal energy kBT. In the interval of the pulling forces f > f* nanoparticle detachment becomes a deterministic process.

Carrillo, Jan-Michael Y.; Dobrynin, Andrey V.

2012-12-01

365

Dynamics of nanoparticle adhesion.  

PubMed

We performed molecular dynamics simulations and theoretical analysis of nanoparticle pulling off from adhesive substrates. Our theoretical model of nanoparticle detachment is based on the Kramers' solution of the stochastic barrier crossing in effective one-dimensional potential well. The activation energy, ?E, for nanoparticle detachment first decreases linearly with increasing the magnitude of the applied force, f, then it follows a power law ?E [proportionality] (f* - f)(3/2) as magnitude of the pulling force f approaches a critical detachment force value, f*. These two different regimes in activation energy dependence on magnitude of the applied force are confirmed by analyzing nanoparticle detachment in effective one-dimensional potential obtained by weighted histogram analysis method. Simulations show that detachment of nanoparticle proceeds through neck formation such that magnitude of the activation energy is determined by balancing surface energy of the neck connecting particle to a substrate with elastic energy of nanoparticle deformation. In this regime the activation energy at zero applied force, ?E(0), for nanoparticle with radius, R(p), shear modulus, G, surface energy, ?(p), and work of adhesion, W, is a universal function of the dimensionless parameter ? [proportionality] ?(p)W(-2/3)(GR(p))(-1/3). Simulation data are described by a scaling function ?E(0) [proportionality] ?(p) (5/2)R(p)(1/2)G(-3/2)?(-3.75). Molecular dynamics simulations of nanoparticle detachment show that the Kramers' approach fails in the vicinity of the critical detachment force f* where activation energy barrier becomes smaller than the thermal energy k(B)T. In the interval of the pulling forces f > f* nanoparticle detachment becomes a deterministic process. PMID:23231258

Carrillo, Jan-Michael Y; Dobrynin, Andrey V

2012-12-01

366

The association between urinary kidney injury molecule 1 and urinary cadmium in elderly during long-term, low-dose cadmium exposure: a pilot study  

PubMed Central

Background Urinary kidney injury molecule 1 is a recently discovered early biomarker for renal damage that has been proven to be correlated to urinary cadmium in rats. However, so far the association between urinary cadmium and kidney injury molecule 1 in humans after long-term, low-dose cadmium exposure has not been studied. Methods We collected urine and blood samples from 153 non-smoking men and women aged 60+, living in an area with moderate cadmium pollution from a non-ferrous metal plant for a significant period. Urinary cadmium and urinary kidney injury molecule 1 as well as other renal biomarkers (alpha1-microglobulin, beta2-microglobulin, blood urea nitrogen, urinary proteins and microalbumin) were assessed. Results Both before (r = 0.20; p = 0.01) and after (partial r = 0.32; p < 0.0001) adjustment for creatinine, age, sex, past smoking, socio-economic status and body mass index, urinary kidney injury molecule 1 correlated with urinary cadmium concentrations. No significant association was found between the other studied renal biomarkers and urinary cadmium. Conclusions We showed that urinary kidney injury molecule 1 levels are positively correlated with urinary cadmium concentration in an elderly population after long-term, low-dose exposure to cadmium, while other classical markers do not show an association. Therefore, urinary kidney injury molecule 1 might be considered as a biomarker for early-stage metal-induced kidney injury by cadmium.

2011-01-01

367

Wet adhesion and adhesive locomotion of snails on anti-adhesive non-wetting surfaces.  

PubMed

Creating surfaces capable of resisting liquid-mediated adhesion is extremely difficult due to the strong capillary forces that exist between surfaces. Land snails use this to adhere to and traverse across almost any type of solid surface of any orientation (horizontal, vertical or inverted), texture (smooth, rough or granular) or wetting property (hydrophilic or hydrophobic) via a layer of mucus. However, the wetting properties that enable snails to generate strong temporary attachment and the effectiveness of this adhesive locomotion on modern super-slippy superhydrophobic surfaces are unclear. Here we report that snail adhesion overcomes a wide range of these microscale and nanoscale topographically structured non-stick surfaces. For the one surface which we found to be snail resistant, we show that the effect is correlated with the wetting response of the surface to a weak surfactant. Our results elucidate some critical wetting factors for the design of anti-adhesive and bio-adhesion resistant surfaces. PMID:22693563

Shirtcliffe, Neil J; McHale, Glen; Newton, Michael I

2012-05-31

368

Wet Adhesion and Adhesive Locomotion of Snails on Anti-Adhesive Non-Wetting Surfaces  

PubMed Central

Creating surfaces capable of resisting liquid-mediated adhesion is extremely difficult due to the strong capillary forces that exist between surfaces. Land snails use this to adhere to and traverse across almost any type of solid surface of any orientation (horizontal, vertical or inverted), texture (smooth, rough or granular) or wetting property (hydrophilic or hydrophobic) via a layer of mucus. However, the wetting properties that enable snails to generate strong temporary attachment and the effectiveness of this adhesive locomotion on modern super-slippy superhydrophobic surfaces are unclear. Here we report that snail adhesion overcomes a wide range of these microscale and nanoscale topographically structured non-stick surfaces. For the one surface which we found to be snail resistant, we show that the effect is correlated with the wetting response of the surface to a weak surfactant. Our results elucidate some critical wetting factors for the design of anti-adhesive and bio-adhesion resistant surfaces.

Shirtcliffe, Neil J.; McHale, Glen; Newton, Michael I.

2012-01-01

369

Caveolin-1 regulates endothelial adhesion of lung cancer cells via reactive oxygen species-dependent mechanism.  

PubMed

The knowledge regarding the role of caveolin-1 (Cav-1) protein on endothelium adhesion of cancer cells is unclear. The present study revealed that Cav-1 plays a negative regulatory role on cancer-endothelium interaction. Endogenous Cav-1 was shown to down-regulate during cell detachment and the level of such a protein was conversely associated with tumor-endothelial adhesion. Furthermore, the ectopic overexpression of Cav-1 attenuated the ability of the cancer cells to adhere to endothelium while shRNA-mediated Cav-1 knock-down exhibited the opposite effect. We found that cell detachment increased cellular hydrogen peroxide and hydroxyl radical generation and such reactive oxygen species (ROS) were responsible for the increasing interaction between cancer cells and endothelial cells through vascular endothelial cell adhesion molecule-1 (VCAM-1). Importantly, Cav-1 was shown to suppress hydrogen peroxide and hydroxyl radical formation by sustaining the level of activated Akt which was critical for the role of Cav-1 in attenuating the cell adhesion. Together, the present study revealed the novel role of Cav-1 and underlying mechanism on tumor adhesion which explain and highlight an important role of Cav-1 on lung cancer cell metastasis. PMID:23460862

Chanvorachote, Pithi; Chunhacha, Preedakorn

2013-02-27

370

Structural specializations of ?4?7, an integrin that mediates rolling adhesion  

PubMed Central

The lymphocyte homing receptor integrin ?4?7 is unusual for its ability to mediate both rolling and firm adhesion. ?4?1 and ?4?7 are targeted by therapeutics approved for multiple sclerosis and Crohn’s disease. Here, we show by electron microscopy and crystallography how two therapeutic Fabs, a small molecule (RO0505376), and mucosal adhesion molecule-1 (MAdCAM-1) bind ?4?7. A long binding groove at the ?4–?7 interface for immunoglobulin superfamily domains differs in shape from integrin pockets that bind Arg-Gly-Asp motifs. RO0505376 mimics an Ile/Leu-Asp motif in ?4 ligands, and orients differently from Arg-Gly-Asp mimics. A novel auxiliary residue at the metal ion–dependent adhesion site in ?4?7 is essential for binding to MAdCAM-1 in Mg2+ yet swings away when RO0505376 binds. A novel intermediate conformation of the ?4?7 headpiece binds MAdCAM-1 and supports rolling adhesion. Lack of induction of the open headpiece conformation by ligand binding enables rolling adhesion to persist until integrin activation is signaled.

Yu, Yamei; Zhu, Jianghai; Mi, Li-Zhi; Walz, Thomas; Sun, Hao; Chen, JianFeng

2012-01-01

371

Focal Adhesion Kinases in Adhesion Structures and Disease  

PubMed Central

Cell adhesion to the extracellular matrix (ECM) is essential for cell migration, proliferation, and embryonic development. Cells can contact the ECM through a wide range of matrix contact structures such as focal adhesions, podosomes, and invadopodia. Although they are different in structural design and basic function, they share common remodeling proteins such as integrins, talin, paxillin, and the tyrosine kinases FAK, Pyk2, and Src. In this paper, we compare and contrast the basic organization and role of focal adhesions, podosomes, and invadopodia in different cells. In addition, we discuss the role of the tyrosine kinases, FAK, Pyk2, and Src, which are critical for the function of the different adhesion structures. Finally, we discuss the essential role of these tyrosine kinases from the perspective of human diseases.

Eleniste, Pierre P.; Bruzzaniti, Angela

2012-01-01

372

Adhesion molecules in tumor metastasis.  

PubMed

It is now clear that adhesive interactions play a critical role in the process of metastatic tumor dissemination. Adhesion molecules act as both positive and negative modulators of the metastatic process. Molecules such as E-cadherin that promote homotypic tumor cell adhesion function to maintain intercellular contacts that confine cells to the primary tumor site and are negatively correlated with metastatic potential. Because tumor cells are rapidly eliminated from the circulation, those cells that can quickly arrest in the vasculature at a secondary site and pass through the vessel wall into the surrounding tissue will have a selective advantage toward establishing new metastatic colonies. The first step in this process is specific adhesion to venular endothelial cells in selected organs, a process mediated by tumor cell surface molecules such as Sialyl LewisX or the VLA-4 (alpha 4 beta 1) integrin that mediate binding to endothelial adhesion molecules such as the E-selectin or the vascular cell adhesion molecule, VCAM-1. Site-specific endothelial determinants such as the lung endothelial cell adhesion molecule, LuECAM, may additionally specify particular sites for preferential adhesion and subsequent site-specific metastasis of particular tumor types. After adherence to endothelial cells and subsequent endothelial retraction, metastatic tumor cells must adhere to elements of the subendothelial basement membrane such as laminin and types IV and V collagen, interactions frequently mediated by members of the beta 1 and beta 4 integrin families. Finally, metastatic tumor cell adhesion to connective tissue elements such as fibronectin, type I collagen and hyaluronan, mediated by molecules such as the beta 1 integrins and by the CD44 cell surface adhesion molecule, are required for movement of tumor cells into the subendothelial stroma and subsequent growth at these new sites. Thus, metastatic potential can be influenced both positively and negatively by a variety of cell surface adhesive molecules that act both independently and in concert to direct tumor cells to particular tissues, allowing them to arrest in those tissues, migrate across the vessel wall and grow at the secondary site. In the current review, I discuss the nature of the adhesion molecules that have been implicated in the metastatic process, emphasizing those molecules that have been shown to correlate with metastasis in clinical human tumors or that have been shown to influence metastatic potential in in vivo experimental assays. PMID:8400144

Zetter, B R

1993-08-01

373

A cannabinoid agonist interferes with the progression of a chronic model of multiple sclerosis by downregulating adhesion molecules.  

PubMed

Adhesion molecules are critical players in the regulation of transmigration of blood leukocytes across the blood-brain barrier in multiple sclerosis (MS). Cannabinoids (CBs) are potential therapeutic agents in the treatment of MS, but the mechanisms involved are only partially known. Using a viral model of MS we observed that the cannabinoid agonist WIN55,212-2 administered at the time of virus infection suppresses intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) in brain endothelium, together with a reduction in perivascular CD4+ T lymphocytes infiltrates and microglial responses. WIN55,212-2 also interferes with later progression of the disease by reducing symptomatology and neuroinflammation. In vitro data from brain endothelial cell cultures, provide the first evidence of a role of peroxisome proliferator-activated receptors gamma (PPARgamma) in WIN55,212-2-induced downregulation of VCAM-1. This study highlights that inhibition of brain adhesion molecules by WIN55,212-2 might underline its therapeutic effects in MS models by targeting PPAR-gamma receptors. PMID:19059482

Mestre, L; Docagne, F; Correa, F; Loría, F; Hernangómez, M; Borrell, J; Guaza, C

2008-11-19

374

Protein Kinase C beta Mediates CD40 Ligand-Induced Adhesion of Monocytes to Endothelial Cells.  

PubMed

Accumulating evidence supports the early involvement of monocyte/macrophage recruitment to activated endothelial cells by leukocyte adhesion molecules during atherogenesis. CD40 and its ligand CD40L are highly expressed in vascular endothelial cells, but its impact on monocyte adhesion and the related molecular mechanisms are not fully understood. The present study was designed to evaluate the direct effect of CD40L on monocytic cell adhesion and gain mechanistic insight into the signaling coupling CD40L function to the proinflammatory response. Exposure of cultured human aortic endothelial cells (HAECs) to clinically relevant concentrations of CD40L (20 to 80 ng/mL) dose-dependently increased human monocytic THP-1 cells to adhere to them under static condition. CD40L treatment induced the expression of vascular cell adhesion molecule-1 (VCAM-1) mRNA and protein expression in HAECs. Furthermore, exposure of HAECs to CD40L robustly increased the activation of protein kinase C beta (PKC?) in ECs. A selective inhibitor of PKC? prevented the rise in VCAM-1 and THP-1 cell adhesion to ECs. Moreover, stimulation of ECs to CD40L induced nuclear factor-?B (NF-?B) activation. PKC? inhibition abolished CD40L-induced NF-?B activation, and NF-?B inhibition reduced expression of VCAM-1, each resulting in reduced THP-1 cell adhesion. Our findings provide the evidence that CD40L increases VCAM-1 expression in ECs by activating PKC? and NF-?B, suggesting a novel mechanism for EC activation. Finally, administration of CD40L resulted in PKC? activation, increased VCAM-1 expression and activated monocytes adhesiveness to HAECs, processes attenuated by PKC? inhibitor. Therefore, CD40L may contribute directly to atherogenesis by activating ECs and recruiting monocytes to them. PMID:24039784

Wu, Zeyu; Zhao, Gang; Peng, Lin; Du, Jialin; Wang, Sanming; Huang, Yijie; Ou, Jinrui; Jian, Zhixiang

2013-09-09

375

Simple Method for Adhesion Measurements.  

National Technical Information Service (NTIS)

An indentation method for determining the adhesion of interfaces between thin films and substrates has been developed. The method provides a quantitative measure of the interface fracture resistance and has the advantage of simplicity and reproducibility....

S. S. Chiang D. B. Marshall A. G. Evans

1980-01-01

376

Seafood delicacy makes great adhesive  

ScienceCinema

Technology from Mother Nature is often hard to beat, so Idaho National Laboratory scientistsgenetically analyzed the adhesive proteins produced by blue mussels, a seafood delicacy. Afterobtaining full-length DNA sequences encoding these proteins, reprod

377

Adhesion of Hydrated Silicate Films.  

National Technical Information Service (NTIS)

We used fracture mechanics test techniques to measure the adhesive bond energy formed between hydrated silica glass surfaces and silicate species deposited from solution. In the case of silicate surfaces hydrated in room temperature water vapor, intermole...

T. A. Michalske K. D. Keefer

1988-01-01

378

Audiofrequency Electrotheraphy in Intestinal Adhesions.  

National Technical Information Service (NTIS)

Audiofrequency electrotherapy (AFET) is used in 140 intestinal adhesion (IA) cases regardless of patient's age, duration of illness, severity of symptoms, number of operations and recurrences and failure of other methods of treatment with 72.8% cures, 18....

1981-01-01

379

Studies of Tannin Formaldehyde Adhesives.  

National Technical Information Service (NTIS)

Tannins are organic complex compounds generally used for tanning different kinds of leather in tanneries. Although there are numerous uses of tannins, the present study is mainly concerned with the preparation of adhesives from tannins. Different solvent ...

M. M. Anwer

1985-01-01

380

Development of Thermoplastic Structural Adhesives.  

National Technical Information Service (NTIS)

Six different classes of thermoplastic polymers having high temperature capabilities (+300 deg F service) were surveyed after studying available data; five polymers from three different classes were screened for adhesive shear properties. The screening wa...

S. G. Hill J. T. Hoggatt

1977-01-01

381

Adhesive interactions between vesicles in the strong adhesion limit  

PubMed Central

We consider the adhesive interaction energy between a pair of vesicles in the strong adhesion limit, in which bending forces play a negligible role in determining vesicle shape compared to forces due to membrane stretching. Although force-distance or energy distance relationships characterizing adhesive interactions between fluid bilayers are routinely measured using the surface forces apparatus, the atomic force microscope and the biomembrane force probe, the interacting bilayers in these methods are supported on surfaces (e.g. mica sheet) and cannot be deformed. However, it is known that in a suspension, vesicles composed of the same bilayer can deform by stretching or bending, and can also undergo changes in volume. Adhesively interacting vesicles can thus form flat regions in the contact zone, which will result in an enhanced interaction energy as compared to rigid vesicles. The focus of this paper is to examine the magnitude of the interaction energy between adhesively interacting, deformed vesicles relative to free, undeformed vesicles as a function of the intervesicle separation. The modification of the intervesicle interaction energy due to vesicle deformability can be calculated knowing the undeformed radius of the vesicles, R0, the bending modulus kb, the area expansion modulus Ka, and the adhesive minimum WP(0) and separation DP(0) in the energy of interaction between two flat bilayers, which can be obtained from the force-distance measurements made using the above supported-bilayer methods. For vesicles with constant volumes, we show that adhesive potentials between non-deforming bilayers such as ?WP(0)??5×10?4mJ/m2, which are ordinarily considered weak in colloidal physics literature, can result in significantly deep (>10×) energy minima due to increase in vesicle area and flattening in the contact region. If the osmotic expulsion of water across the vesicles driven by the tense, stretched membrane in the presence of an osmotically active solute is also taken into account, the vesicles can undergo additional deformation (flattening), which further enhances the adhesive interaction between them. Finally, equilibration of ions and solutes due to the concentration differences created by the osmotic exchange of water can lead to further enhancement of the adhesion energy. Our result of the progressively increasing adhesive interaction energy between vesicles in above regimes could explain why suspensions of very weakly attractive vesicles may undergo flocculation and eventual instability due to separation of vesicles from the suspending fluid by gravity. The possibility of such an instability is an extremely important issue for concentrated vesicle-based products and applications such as fabric softeners, hair therapeutics and drug delivery.

Ramachandran, Arun; Anderson, Travers H.; Leal, L. Gary; Israelachvili, Jacob N.

2010-01-01

382

A method for testing denture adhesives.  

PubMed

An in vitro test method is described simulating the in vivo fate of a denture adhesive, i.e., destruction of the adhesive, dilution, and dissolution, by measuring the bond strength for the adhesive placed between acrylic resin plates. Between each measurement, the adhesive was exposed to isotonic saline. The bond strength for two ointment denture adhesives, Super Corega and Fixodent, was measured and the results were compared with those obtained for one of them in a previous in vivo test. The test method described for denture adhesives seems useful to depict the fate of a denture adhesive in clinical use. PMID:1791561

Fløystrand, F; Koppang, R; Williams, V D; Orstavik, J

1991-10-01

383

Leukostasis and pigment epithelium-derived factor in rat models of diabetic retinopathy  

PubMed Central

Purpose Spontaneously diabetic Torii (SDT) rats, an animal model of type 2 diabetes, have a low incidence of neovascular formation and an absence of non-perfused areas in their retinas at the proliferative stage that presents tractional retinal detachment with fibrous proliferation. The aim of this study was to determine whether leukostasis is present in the retina, to evaluate the levels of pigment epithelium-derived factor (PEDF) and intracellular adhesion molecule-1 (ICAM-1) levels in the blood of SDT rats, and to examine the effects of PEDF on leukostasis. Methods SDT rats, streptozotocin-induced diabetic (STZ) rats, and control Sprague-Dawley (SD) rats were studied. The index of leukostasis in the retina was determined immunohistochemically by counting the number of labeled adherent leukocytes. The levels of PEDF and the soluble intracellular adhesion molecule (sICAM)-1 in the plasma were measured. To investigate the effect of PEDF and vascular endothelial growth factor (VEGF) on leukostasis, the adhesion of monocytes to human umbilical vein endothelial cells (HUVECs) was assayed in vitro. Results SDT and STZ diabetic rats showed a significant increase of retinal leukostasis compared to that of control SD rats, but SDT rats had noteworthy lower levels of leukostasis than STZ rats in long term experiments. The sICAM-1 levels and PEDF expression were up-regulated in both STZ and SDT rats, but the SDT rats showed significantly higher levels of PEDF than STZ rats. In vitro studies showed that exposure of HUVECs to VEGF increased the number of adhering monocytes, and PEDF inhibited the VEGF-induced leukostasis in a dose-dependent manner. Conclusions The inhibition of the VEGF-induced leukostasis by PEDF is most likely responsible for the low incidence of capillary occlusion and retinal neovascularization in SDT rats.

Matsuoka, Masato; Minamino, Keizo; Matsumura, Miyo

2007-01-01

384

Effects of adhesive fillers on the strength of tubular single lap adhesive joints  

Microsoft Academic Search

When an adhesively bonded joint is exposed to a high environmental temperature, the tensile load capability of the adhesively bonded joint decreases because the elastic modulus and failure strength of the adhesive decrease. In this paper, the elastic modulus and failure strength of the adhesive as well as the tensile load capability of the tubular single lap adhesively bonded joint

Dai Gil Lee; Jin Kook Kim; Durk Hyun Cho

1999-01-01

385

Integrin-mediated adhesion complex  

PubMed Central

The integrin-mediated adhesion machinery is the primary cell-matrix adhesion mechanism in Metazoa. The integrin adhesion complex, which modulates important aspects of the cell physiology, is composed of integrins (alpha and beta subunits) and several scaffolding and signaling proteins. Integrins appeared to be absent in all non-metazoan eukaryotes so-far analyzed, including fungi, plants and choanoflagellates, the sister-group to Metazoa. Thus, integrins and, therefore, the integrin-mediated adhesion and signaling mechanism was considered a metazoan innovation. Recently, a broad comparative genomic analysis including new genome data from several unicellular organisms closely related to fungi and metazoans shattered previous views. The integrin adhesion and signaling complex is not specific to Metazoa, but rather it is present in apusozoans and holozoan protists. Thus, this important signaling and adhesion system predated the origin of Fungi and Metazoa, and was subsequently lost in fungi and choanoflagellates. This finding suggests that cooption played a more important role in the origin of Metazoa than previously believed. Here, we hypothesize that the integrin adhesome was ancestrally involved in signaling.

Sebe-Pedros, Arnau

2010-01-01

386

Glutathione peroxidase-1 modulates lipopolysaccharide-induced adhesion molecule expression in endothelial cells by altering CD14 expression  

PubMed Central

CD14 contributes to LPS signaling in leukocytes through formation of toll-like receptor 4/CD14 receptor complexes; however, a specific role for endogenous cell-surface CD14 in endothelial cells is unclear. We have found that suppression of glutathione peroxidase-1 (GPx-1) in human microvascular endothelial cells increases CD14 gene expression compared to untreated or siControl (siCtrl)-treated conditions. Following LPS treatment, GPx-1 deficiency augmented LPS-induced intracellular reactive oxygen species accumulation, CD14 expression, and intercellular adhesion molecule-1 (ICAM-1) mRNA and protein expression compared to LPS-treated control cells. GPx-1 deficiency also transiently augmented LPS-induced vascular cell adhesion molecule-1 (VCAM-1) expression. Adenoviral overexpression of GPx-1 significantly diminished LPS-mediated responses in adhesion molecule expression. Consistent with these findings, LPS responses were also greater in endothelial cells derived from GPx-1-knockout mice, whereas adhesion molecule expression was decreased in cells from GPx-1-overexpressing transgenic mice. Knockdown of CD14 attenuated LPS-mediated up-regulation of ICAM-1 and VCAM-1 mRNA and protein, and it mitigated the effects of GPx-1 deficiency on LPS-induced adhesion molecule expression. Taken together, these data suggest that GPx-1 modulates the endothelial cell response to LPS, in part, by altering CD14-mediated effects.—Lubos, E., Mahoney, C. E., Leopold, J. A., Zhang, Y.-Y., Loscalzo, J., Handy, D. E. Glutathione peroxidase-1 modulates lipopolysaccharide-induced adhesion molecule expression in endothelial cells by altering CD14 expression.

Lubos, Edith; Mahoney, Christopher E.; Leopold, Jane A.; Zhang, Ying-Yi; Loscalzo, Joseph; Handy, Diane E.

2010-01-01

387

Induction of heme oxygenase 1 by arsenite inhibits cytokine-induced monocyte adhesion to human endothelial cells  

SciTech Connect

Heme oxygenase-1 (HO-1) is an oxidative stress responsive gene upregulated by various physiological and exogenous stimuli. Arsenite, as an oxidative stressor, is a potent inducer of HO-1 in human and rodent cells. In this study, we investigated the mechanistic role of arsenite-induced HO-1 in modulating tumor necrosis factor {alpha} (TNF-{alpha}) induced monocyte adhesion to human umbilical vein endothelial cells (HUVEC). Arsenite pretreatment, which upregulated HO-1 in a time- and concentration-dependent manner, inhibited TNF-{alpha}-induced monocyte adhesion to HUVEC and intercellular adhesion molecule 1 protein expression by 50% and 40%, respectively. Importantly, knockdown of HO-1 by small interfering RNA abolished the arsenite-induced inhibitory effects. These results indicate that induction of HO-1 by arsenite inhibits the cytokine-induced monocyte adhesion to HUVEC by suppressing adhesion molecule expression. These findings established an important mechanistic link between the functional monocyte adhesion properties of HUVEC and the induction of HO-1 by arsenite.

Sun Xi [College of Pharmacy, MSC09 5360, 1 University of New Mexico, Albuquerque, NM 87131-0001 (United States); Pi Jingbo [Division of Translational Biology, Hamner Institutes for Health Sciences, Research Triangle Park, NC 27709 (United States); Liu Wenlan; Hudson, Laurie G.; Liu Kejian [College of Pharmacy, MSC09 5360, 1 University of New Mexico, Albuquerque, NM 87131-0001 (United States); Feng Changjian [College of Pharmacy, MSC09 5360, 1 University of New Mexico, Albuquerque, NM 87131-0001 (United States)], E-mail: cfeng@salud.unm.edu

2009-04-15

388

Ginsenoside rg2 inhibits lipopolysaccharide-induced adhesion molecule expression in human umbilical vein endothelial cell.  

PubMed

Vascular cell adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), P- and E-selectin play a pivotal role for initiation of atherosclerosis. Ginsenoside, a class of steroid glycosides, is abundant in Panax ginseng root, which has been used for prevention of illness in Korea. In this study, we investigated the mechanism(s) by which ginsenoside Rg2 may inhibit VCAM-1 and ICAM-1 expressions stimulated with lipopolysaccharide (LPS) in human umbilical vein endothelial cell (HUVEC). LPS increased VCAM-1 and ICAM-1 expression. Ginsenoside Rg2 prevented LPS-mediated increase of VCAM-1 and ICAM-1 expression. On the other hand, JSH, a nuclear factor kappa B (NF-?B) inhibitor, reduced both VCAM-1 and ICAM-1 expression stimulated with LPS. SB202190, inhibitor of p38 mitogen-activated protein kinase (p38 MAPK), and wortmannin, phosphatidylinositol 3-kinase (PI3-kinase) inhibitor, reduced LPS-mediated VCAM-1 but not ICAM-1 expression. PD98059, inhibitor of mitogen-activated protein kinase kinase/extracellular signal-regulated kinase (MEK/ERK) did not affect VCAM-1 and ICAM-1 expression stimulated with LPS. SP600125, inhibitor of c-Jun N-terminal kinase (JNK), reduced LPS-mediated ICAM-1 but not VCAM-1 expression. LPS reduced IkappaB? (I?B?) expression, in a time-dependent manner within 1 hr. Ginsenoside Rg2 prevented the decrease of I?B? expression stimulated with LPS. Moreover, ginsenoside Rg2 reduced LPS-mediated THP-1 monocyte adhesion to HUVEC, in a concentration-dependent manner. These data provide a novel mechanism where the ginsenoside Rg2 may provide direct vascular benefits with inhibition of leukocyte adhesion into vascular wall thereby providing protection against vascular inflammatory disease. PMID:23626475

Cho, Young-Suk; Kim, Chan Hyung; Ha, Tae-Sun; Lee, Sang Jin; Ahn, Hee Yul

2013-04-10

389

Ginsenoside Rg2 Inhibits Lipopolysaccharide-Induced Adhesion Molecule Expression in Human Umbilical Vein Endothelial Cell  

PubMed Central

Vascular cell adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), P- and E-selectin play a pivotal role for initiation of atherosclerosis. Ginsenoside, a class of steroid glycosides, is abundant in Panax ginseng root, which has been used for prevention of illness in Korea. In this study, we investigated the mechanism(s) by which ginsenoside Rg2 may inhibit VCAM-1 and ICAM-1 expressions stimulated with lipopolysaccharide (LPS) in human umbilical vein endothelial cell (HUVEC). LPS increased VCAM-1 and ICAM-1 expression. Ginsenoside Rg2 prevented LPS-mediated increase of VCAM-1 and ICAM-1 expression. On the other hand, JSH, a nuclear factor kappa B (NF-?B) inhibitor, reduced both VCAM-1 and ICAM-1 expression stimulated with LPS. SB202190, inhibitor of p38 mitogen-activated protein kinase (p38 MAPK), and wortmannin, phosphatidylinositol 3-kinase (PI3-kinase) inhibitor, reduced LPS-mediated VCAM-1 but not ICAM-1 expression. PD98059, inhibitor of mitogen-activated protein kinase kinase/extracellular signal-regulated kinase (MEK/ERK) did not affect VCAM-1 and ICAM-1 expression stimulated with LPS. SP600125, inhibitor of c-Jun N-terminal kinase (JNK), reduced LPS-mediated ICAM-1 but not VCAM-1 expression. LPS reduced IkappaB? (I?B?) expression, in a time-dependent manner within 1 hr. Ginsenoside Rg2 prevented the decrease of I?B? expression stimulated with LPS. Moreover, ginsenoside Rg2 reduced LPS-mediated THP-1 monocyte adhesion to HUVEC, in a concentration-dependent manner. These data provide a novel mechanism where the ginsenoside Rg2 may provide direct vascular benefits with inhibition of leukocyte adhesion into vascular wall thereby providing protection against vascular inflammatory disease.

Cho, Young-Suk; Kim, Chan Hyung; Ha, Tae-Sun; Lee, Sang Jin

2013-01-01