Platelet Activation and Blood Coagulation
Platelet Activation and Blood Coagulation
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DOI：
10.1055/s-0037-1613209
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发表时间：
2002-08
影响因子：
6.7
通讯作者：
J. Heemskerk;E. Bevers;T. Lindhout
中科院分区：
文献类型：
--
作者：
J. Heemskerk;E. Bevers;T. Lindhout
摘要 在止血和血栓形成过程中，血小板活化和血液凝固是互补的、相互依赖的过程。血小板与多种凝血因子相互作用，而凝血产物凝血酶是一种有效的血小板激活剂。胞质 [Ca2+]i 长期升高后，活化的血小板进入促凝血状态。这样的血小板，例如。 g。当通过糖蛋白 VI 粘附到胶原蛋白上时，在其外表面暴露磷脂酰丝氨酸 (PS) 并产生（暴露 PS）膜泡和微泡。氨基磷脂转位酶的抑制和磷脂扰乱酶的激活介导 PS 的暴露，而钙蛋白酶介导的蛋白质裂解导致膜起泡和囊泡形成。表面暴露的 PS 通过促进 tenase 和凝血酶原酶复合物的组装和激活来强烈促进凝血过程。因子 IXa 和血小板结合因子 Va 支持这些活性。此外，血小板可以通过提供凝血酶原和因子 XI 的结合位点来支持凝血的起始阶段。因此，它们接管了组织因子和因子 VIIa 在凝血激活中的起始作用。
Summary Platelet activation and blood coagulation are complementary, mutually dependent processes in haemostasis and thrombosis. Platelets interact with several coagulation factors, while the coagulation product thrombin is a potent platelet-activating agonist. Activated platelets come in a procoagulant state after a prolonged elevation in cytosolic [Ca2+]i. Such platelets, e. g. when adhering to collagen via glycoprotein VI, expose phosphatidylserine (PS) at their outer surface and produce (PS-exposing) membrane blebs and microvesicles. Inhibition of aminophospholipid translocase and activation of phospholipid scramblase mediate the exposure of PS, whereas calpain-mediated protein cleavage leads to membrane blebbing and vesiculation. Surface-exposed PS strongly propagates the coagulation process by facilitating the assembly and activation of tenase and prothrombinase complexes. Factor IXa and platelet-bound factor Va support these activities. In addition, platelets can support the initiation phase of coagulation by providing binding sites for prothrombin and factor XI. They thereby take over the initiating role of tissue factor and factor VIIa in coagulation activation.