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目的:研究LSA引起信号传递以及PLC 2诱导的血小板聚集和分泌的作用。方法:通过酶联免疫吸附配体-受体结合及血小板聚集和分泌实验,研究LSA诱导血小板活化的作用及参与的信号分子。结果:LSA引起了整合素Ⅱb 3上LIBS表位表达明显增加,PLC 2可能以一种酪氨酸活化依赖性的方式参与了这种信号传递。结论:LSA引起的信号传递是由β3介导的,并且LSA可引起不依赖于聚集的活化剂的分泌,而这些活化剂能引发聚集依赖性Ⅱb 3信号传递。
AIM: To investigate the role of LSA in signal transduction and platelet aggregation and secretion induced by PLC 2. METHODS: The effects of LSA on platelet activation and the involved signaling molecules were studied by enzyme-linked immunosorbent ligand-receptor binding and platelet aggregation and secretion assays. RESULTS: LSA caused a significant increase in LIBS epitope expression on integrin IIb 3, which may be involved in a tyrosine activation-dependent manner. CONCLUSIONS: LSA-induced signaling is mediated by β3 and LSA can induce secretion independent of aggregation-independent activators that trigger aggregation dependent IIb3 signaling.