流场中vWF-A1介导的血小板表面CD40L表达

The VWF-A1-Mediated Platelet Surface CD40L Expression in Flow Field

目的揭示流场中vWF-A1介导血小板表面CD40L表达的力学调控机制。方法选用原核系统表达蛋白、流式细胞仪、平行平板流动腔技术与细胞免疫荧光抗体染色技术,探究在不同流体剪切力(fluid shear stress,FSS)环境中血小板由vWF-A1诱导活化和随后表达CD40L的过程。结果vWF-A1在静息条件下不会激活血小板;FSS是vWF-A1介导的血小板CD40L表达的启动开关;随着剪切应力累积(shear stress accumulation,SSA)的增加,血小板CD40L的表达水平呈现先上升后下降的趋势,当SSA达到2 Pa·min时,血小板CD40L表达量达到峰值。结论vWF-A1、FSS和SSA调控血小板表面CD40L的表达,SSA促进了血小板表达CD40L的能力。

Objective To reveal the mechanism of mechanical regulation of platelet surface CD40L expression mediated by vWF-A1 in flow filed.Methods The prokaryotic systems expressing proteins,flow cytometry,and parallel plate flow chamber technique with cellular immunofluorescent antibody staining were selected,so as to investigate the activation and subsequent expression of CD40L induced by vWF-A1 in platelets under different fluid shear stress(FSS)environments.Results The vWF-A1 did not activate platelets under resting conditions.FSS was the initiating switch for vWF-A1-mediated platelet CD40L expression.With the increase of shear stress accumulation(SSA),the expression level of platelet CD40L showed a trend of increasing and then decreasing,and when SSA reached 2 Pa·min,the expression of platelet CD40L reached its peak.Conclusions The expression of CD40L on platelet surface is regulated by vWF-A1,FSS and SSA.SSA promote the ability of platelets to express CD40L.