Intercellular Adhesion Molecule 1 (ICAM-1) Gene Variant Is Associated with Coronary Artery Calcification Independent of Soluble ICAM-1 Levels
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The dual radiolabeled mAb technique was used to quantify the constitutive and induced expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in the microvasculature of different organs of the mouse. The constitutive expression of both adhesion molecules varied significantly between tissues, with ICAM-1 levels consistently higher than VCAM-1 in all tissues studied. Following systemic administration of endotoxin (LPS), an increased surface expression of both adhesion molecules occurred in most organs, with the largest increases for ICAM-1 (2 to 3x increase) noted in the heart, small intestine, and brain, while heart and small intestine exhibited the largest increases in LPS-induced VCAM-1 expression (2 to 5x increase). These responses occurred in the face of an unaltered expression of platelet endothelial cell adhesion molecule-1 (PECAM-1) in all tissues. TNF-alpha also elicited an increased expression of both adhesion molecules, with initial increases noted at 2 to 5 h, peak levels at 5 to 9 h, and a sustained elevation above baseline at 24 h. The TNF-alpha-induced increases in both ICAM-1 and VCAM-1 were dose dependent, with significant up-regulation noted at 5 microg/kg and maximal increases occurring at 10 to 25 microg/kg. These studies indicate that while there are significant quantitative differences in constitutive and induced expression of murine ICAM-1 and VCAM-1, the kinetics and dose-response characteristics of the two adhesion molecules to TNF-alpha are qualitatively similar.
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Objective: To investigate PYM-regulated expressions of VCAM-1,ICAM-1 and ICAM-3 in primary cultured HVMECs.Methods: Expressions of the adhesion molecules VCAM-1,ICAM-1 and ICAM-3 were studied in PYM-regulated HVMECs in vitro by means of ELISA and RT-PCR.Results: Expressions of VCAM-1 and ICAM-3 were induced,and expression of ICAM-1 was up-regulated,both in a time and concentration-dependent fashion after stimulation with PYM.The expression of VCAM-1 was observed at 2h and ICAM-1 at 6h and ICAM-3 at 12h.The highest expression of VCAM-1,ICAM-1 and ICAM-3 was observed at 8h,18h and 24h.After exposed for the same time interval,expression of adhesion molecules on HVMECs exposed to 1mg/L of PYM was higher than that exposed to other concentration of PYM.mRNA expressions of VCAM-1,ICAM-1 and ICAM-3 started at 2h,6h and 12h respectively.Maximal synthetic activity was observed at 6-8h for VCAM-1,at 12-18h for ICAM-1 and at 18-24h for ICAM-3.Synthesis activity was greatly suppressed at 10mg/L or higher concentration.Conclusion: Expression of Ig-like adhesion molecules in HVMECs can be induced or up-regulated by lower concentration of PYM in a time and concentration-dependent fashion.
VCAM-1
Intercellular adhesion molecule
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Intercellular adhesion molecules 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCM-l) play important roles in the inflammatory process of cerebral ischemic injury. The expression of ICAM-l and VCAM-1 increases following cerebral ischemia; ICAM1 and VCAM-l promote ischemic inflammation through mediating leukocytes adhesion to the endothelial cells and eventually migration into brain tissue; the inhibition of the overexpression and effect of ICAM-l and VCAM-l can reduce cerebral ischemic injury.
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Microangiopathy
Intercellular adhesion molecule
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Ezrin is a cytoplasmic linker molecule between plasma membrane components and the actin-containing cytoskeleton. We studied whether ezrin is associated with intercellular adhesion molecule (ICAM)-1, -2, and -3. In transfected cells, ICAM-1 and ICAM-2 colocalized with ezrin in microvillar projections, whereas an ICAM-1 construct attached to cell membrane via a glycophosphatidylinositol anchor was uniformly distributed on the cell surface. An interaction of ICAM-2 and ezrin was seen by affinity precipitation, microtiter binding assay, coimmunoprecipitation, and surface plasmon resonance methods. The calculatedKD value was 3.3 × 10−7m. Phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2) induced an interaction of ezrin and ICAM-1 and enhanced the interaction of ezrin and ICAM-2, but ICAM-3 did not bind ezrin even in the presence of PtdIns(4,5)P2. PtdIns(4,5)P2 was shown to bind to cytoplasmic tails of ICAM-1 and ICAM-2, which are the first adhesion proteins demonstrated to interact with PtdIns(4,5)P2. The results indicate an interaction of ezrin with ICAM-1 and ICAM-2 and suggest a regulatory role of phosphoinositide signaling pathways in regulation of ICAM-ezrin interaction.
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