Platelet-cell adhesion

YIGSR, IKVAV (from laminin) REDV (endotheUal-specilic) Adhesion molecules Intercellular adhesion molecule-1 (ICAM-I) Vascular cell adhesion molecule-1 (VCAM-l) Platelet cell adhesion molecule-1 (PCAM-1)... 

Cell Adhesion. The membranes of leukocytes and platelets contain a variety of components that promote ceU-surface contact. Although numerous ceU-surface molecules are likely to play a role in ceU-surface adhesion, the group of selectins are of particular interest to research on this subject. Selectins are molecules that are known to promote leukocyte—platelet adhesion. However, selectin-based models have not been able to account for the fact that platelets are allowed to pass through the filter and leukocytes are not. 

Key PMN, polymorphonuclear leukocytes EC, endothelial cell lymphs, lymphocytes CD, cluster of differentiation iCAM, intercellular adhesion molecule LFA-1, lymphocyte function-associated antigen-1 PECAM-1, platelet endothelial cell adhesion cell molecule-1. 

PE Phosphatidylethanolamine PECAM-1 Platelet endothelial cell adhesion molecule-1 also known as CD31... 

The first aspect of biocompatibility is a natural immune response. When a foreign object enters the blood stream, it can be attacked by the body s defense system. The first step is protein adsorption on an object surface. It is believed that the amount and type of protein adsorption is one of the most important steps determining whether the object is tolerated or rejected by the body. The next step is cell adhesion, which may cause aggregation and activation of platelets and triggering of the blood coagulation system with resulting thrombus formation. It may not only lead to sensor failure via surface blocking but directly threatens the patient s health. 

Some active materials are carriers for drugs (drug delivery systems), some have immobilized peptides to enable cell adhesion or migration, some are degradable by hydrolysis or by specific enzyme action. Some contain bioactive agents (e.g., heparin, thrombomodulin) to prevent coagulation or platelet activation while others incorporate bioactive groups to enhance osteo-conduction. Many include polyethylene oxide to retard protein adsorption and this is perhaps the closest we have come to a kind of inertness. 

DETA/NO is a stable NO-donor with the longest NO generation half-life of approximately 20 h. Thrombelastography performed on rabbit blood showed that DETA NONOate-derived NO significantly decreased coagulation activity and platelet activation [48]. Monitoring by intravital microscopy showed that DETA/NO attenuated the platelets/endothelial cells adhesion response to endotoxins (e.g. lipopolysaccharides) in murine intestinal venules [49]. The main mechanism of the antiadhesive action of DETA/NO on platelets was activation of soluble guanylate cyclase [49]. 

ICAM-1, ICAM-2) and vascular cell adhesion molecule (VCAM). Platelets are attracted to damaged endothelium where they adhere to prevent blood loss in a similar fashion to white blood cells, i.e. via adhesion molecule interactions, to form a clot (thrombus). 

Therapeutic irradiation is known to have multiple interactions with the vasculature of the irradiated tissue (12). Radiation has direct cytotoxic effects on the vascular endothelium, likely due to induction of oxidative injury. Radiation-induced injury stimulates inflammation and influx of inflammatory cells in addition to creating aprocoagulant state in the vascular space by the transcriptional induction of tissue factor with the subsequent activation of coagulation factors as well as von Willebrand factor and platelets. Experimental evidence suggests that the mechanism by which radiation initiates these responses is in part through the induction of cell-adhesion molecules including ICAM-1, E-selectin, and P-selectin and in part through local cytokine production and release (13). 

The physiological function of heparin is not completely understood. It is found only in trace amounts in normal circulating blood. It exerts an antihpemic effect by releasing lipoprotein lipase from endothehal cells heparinlike proteoglycans produced by endothelial cells have anticoagulant activity. Heparin decreases platelet and inflammatory cell adhesiveness to endothelial cells, reduces the release of platelet-derived growth factor, inhibits tumor cell metastasis, and exerts an antiproliferative effect on several types of smooth muscle. 

Pellegatta, R Chierchia, S.L. Zocchi, M.R. Functional association of platelet endothelial cell adhesion molecule-1 and phosphoinositide 3-kinase in human neutrophils. J. Biol. Chem., 273, 27768-27771 (1998)... 

Kroll H, Sun QH, Santoso S. Platelet endothelial cell adhesion molecule-1 (PECAM-1) is a target glycoprotein in drug-induced thrombocytopenia. Blood 2000 96(4) 1409-14. 

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