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,探究在不同剪切力环境中血小板由 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;流体剪切力( fluid shear stress,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。

bjective 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 shear environments. Results The vWF-A1 did not activate platelets under resting conditions. Fluid shear stress (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.

国家自然科学基金项目(12072117,12172137)