Andrews R K, Berndt M C
Hazel and Pip Appel Vascular Biology Laboratory, Baker Medical Research Institute, Prahran, Australia.
Histol Histopathol. 1998 Jul;13(3):837-44. doi: 10.14670/HH-13.837.
Cell-cell and cell-extracellular matrix adhesion are critical aspects of platelet function, regulating interactions between circulating platelets in the bloodstream with the blood vessel wall. In haemostasis, platelets adhere to the subendothelial matrix of a damaged vessel, spread over the surface and recruit additional platelets within a developing platelet aggregate or thrombus. In addition to this normal physiological response, platelet adhesion is critical in the pathological process of thrombosis, where circulating platelets adhere to sclerotic lesions or undergo shear-induced aggregation within vessels occluded by atherosclerotic plaque. Under these circumstances, the resulting thrombus may result in acute myocardial infarction or stroke. Each stage of platelet adhesion and aggregation in haemostasis and thrombosis is regulated by specific cell surface adhesion receptors. Interestingly, most of the adhesive receptors studied in detail have been found not only to regulate contact adhesion, but also to transduce intracellular signals that activate the cell, initiate post-adhesion cellular events, and regulate the adhesive function of other receptors. Platelet activation triggers the cytoskeletal rearrangements that control cell shape change, spreading, secretion, aggregation and contraction. This review will focus on adhesion-dependent signalling induced by the platelet surface receptor, the glycoprotein (GP) Ib-IX-V complex, that initiates thrombus formation in both haemostasis and thrombosis under conditions of high shear blood flow. Emerging evidence suggests GP Ib-IX-V-dependent signalling may involve receptor cross-linking and the cytoplasmic signalling protein, 14-3-3 zeta.
细胞间和细胞与细胞外基质的黏附是血小板功能的关键方面，调节血流中循环血小板与血管壁之间的相互作用。在止血过程中，血小板黏附于受损血管的内皮下基质，在其表面铺展，并在正在形成的血小板聚集体或血栓内募集更多血小板。除了这种正常的生理反应外，血小板黏附在血栓形成的病理过程中也至关重要，在这一过程中，循环血小板黏附于硬化病变处，或在被动脉粥样硬化斑块阻塞的血管内发生剪切诱导的聚集。在这些情况下，形成的血栓可能导致急性心肌梗死或中风。止血和血栓形成过程中血小板黏附和聚集的每个阶段都由特定的细胞表面黏附受体调节。有趣的是，详细研究的大多数黏附受体不仅调节接触黏附，还能转导激活细胞的细胞内信号，启动黏附后细胞事件，并调节其他受体的黏附功能。血小板活化触发细胞骨架重排，控制细胞形状变化、铺展、分泌、聚集和收缩。本综述将聚焦于由血小板表面受体糖蛋白（GP）Ib-IX-V复合物诱导的黏附依赖性信号传导，该复合物在高剪切血流条件下启动止血和血栓形成过程中的血栓形成。新出现的证据表明，GP Ib-IX-V依赖性信号传导可能涉及受体交联和细胞质信号蛋白14-3-3ζ。
