作者: Thomas Bombeli , Barbara R. Schwartz , John M. Harlan
DOI: 10.1182/BLOOD.V93.11.3831
关键词:
摘要: Under normal conditions, platelets do not adhere to endothelium. However, when or endothelial cells are stimulated by thrombin cytokines, respectively, bind avidly Because there is accumulating evidence that may become apoptotic under certain proinflammatory prothrombotic we investigated whether undergoing apoptosis proadhesive for nonactivated platelets. Human umbilical vein (HUVEC) were induced undergo staurosporine, a nonspecific protein kinase inhibitor, culture in suspension with serum-deprivation. After treatment of HUVEC different receptor antagonists, nonactivated, washed human allowed 20 minutes. To exclude matrix involvement, platelet binding was measured using flow cytometry. Independent the method induction, marked increase HUVEC. Although exhibited maximal adhesiveness after 2 4 hours, complete DNA fragmentation occurred only several hours later. Adhesion assays blockade receptors showed involvement beta1-integrins. Platelet inhibited more than 70% treated blocking anti-beta1 antibodies. Treatment antibodies potential receptors, including known ligands beta1-integrins, did affect binding. As assessed determination beta-thromboglobulin and factor supernatants, bound became slightly activated. significant expression P-selectin (CD62P) found. These data provide further contribute thrombotic events.