THE COAGULATION CASCADE - INITIATION, MAINTENANCE, AND REGULATION
THE COAGULATION CASCADE - INITIATION, MAINTENANCE, AND REGULATION
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DOI：
10.1021/bi00107a001
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发表时间：
1991-10-29
期刊：
影响因子：
2.9
通讯作者：
KISIEL, W
中科院分区：
文献类型：
--
作者：
DAVIE, EW;FUJIKAWA, K;KISIEL, W
生物化学系，华盛顿大学，西雅图，华盛顿98195，血液系统研究基金会实验室，病理学系，新墨西哥州医学院，阿尔伯克基，新墨西哥州87131，1991年7月22日接收; 1991年9月3日收到的修订手册中有两种主要的机制来阻止高等生物在血管损伤后的失血。最初，小板被激活并粘附到损伤部位。然后血小板聚集并形成血小板栓，其减少或暂时停止失血。血小板的活化也释放大量蛋白质和小分子，这些蛋白质和小分子加速和增加血小板栓形成，并开始组织修复过程（Majerus，1987）。血浆蛋白如von Willebrand因子通过在活化的血小板和内皮下之间形成桥而在血小板粘附中起重要作用（Girma等人，1987; Ruggeri &齐默尔曼，1987）。这是通过冯维勒布兰德因子与活化血小板表面上的特异性受体（糖蛋白Ib/糖蛋白IX）以及内皮下的结合来实现的（洛佩斯等人，1988; Hickey等人，1989年）。以类似的方式，纤维蛋白原通过与相邻活化血小板上的表面受体（糖蛋白IIb/IIIa）结合而在活化血小板之间形成桥（班尼特等人，一九八二年;
Department of Biochemistry, University of Washington, Seattle, Washington 98195, and Blood Systems Research Foundation Laboratory, Department of Pathology, University of New Mexico School of Medicine, Albuquerque, New Mexico 87131 Received July 22, 1991; Revised Manuscript Received September 3, 1991 ere are two principal mechanisms to stop the loss of blood in higher organisms following vascular injury. Initially, plate-lets are activated and adhere to the site of injury. The platelets then aggregate and form a platelet plug that reduces or tem-porarily stops the loss of blood. The activation of platelets also releases numerous proteins and small molecules that accelerate and increase platelet plugformation and begin the process of tissue repair (Majerus, 1987). Plasma proteins such as von Willebrand factor play an important rolein platelet adhesion by forming a bridge between the activated platelet and the subendothelium (Girma et al., 1987; Ruggeri & Zimmerman, 1987). This is accomplished by the binding of von Willebrand factor to specific receptors (glycoprotein Ib/glycoprotein IX) on the surface of the activated platelets as well as to the subendothelium (Lopez et al., 1988; Hickey et al., 1989). In a similar manner, fibrinogen forms a bridge between activated platelets by binding to the surface receptors (glycoprotein Ilb/llla) on adjacent activated platelets (Bennett et al., 1982;