剪切应力诱导血小板聚集

剪切应力诱导血小板聚集（shear-induced platelet aggregation, SIPA）是指在高剪切流场诱导下血小板表面的膜糖蛋白（GPⅠb/Ⅸ/Ⅴ和GPⅡb/Ⅲa）与血浆中的von Willebrand因子（vWF）相结合，介导血小板的活化、黏附和聚集，是动脉血栓的重要成因.SIPA还需要Ca2+,ADP/ATP等生化因素的参与，因而SIPA现象是生化因素和力学因素偶合作用的结果.细胞外Ca2+是高剪切应力诱导血小板发生聚集的必需条件，Ca2+的跨膜内流引起细胞骨架结构的改变和GPⅡb/Ⅲa的活化.近来对ADP/ATP位于血小板膜上的P2受体的研究表明，P2受体与细胞内Ca2+协同作用通过多种生化途径调控血小板的活化过程在SIPA的信号传导中起着关键的作用.从力学环境与生化反应的偶合关系入手研究SIPA现象的触发机制，深入研究SIPA现象中的信号转导通路是今后的研究热点之一.

Shear-induced Platelet Aggregation

Shear-induced platelet aggregation (SIPA) is an important phenomenon in arterial thrombogenesis. High shear stress triggers von Willebrand factor (vWF) binding to platelet membrane glycoproteins Ⅰb and subsequent platelet activation, adhesion and aggregation. On the contrary, no SIPA phenomenon was found under low shear flow. Therefore, SIPA is a special coupled process involving of biochemistry and fluid mechanic factors. Ca2+, especially extracellular Ca2+, and nucleotides (ADP/ATP) are known to the inducer of SIPA. Ca2+ flux triggers cytoskeletal rearrangement and GPⅡb/Ⅲa activation. Recent studies indicate that P2 receptors for ADP and ATP mediate the Ca2+ influx signal and intracellular Ca2+ mobilization. Furthermore, P2 receptors with Ca2+，which play a key role in the signal transmission in SIPA, induces platelet activation via different pathways. These investigations shed light for understanding complex molecular mechanism of SIPA.