内皮祖细胞（EPCs）可分化为成熟内皮细胞，参与损伤血管的再内皮化及缺血性病变的血管新生。切应力条件下 EPCs 的 microRNAs（miRs）是否参与调控 EPCs 功能及内膜损伤修复，这一机制尚不清楚。本研究拟采用平行平板流动腔模型，应用miRs芯片和表达谱芯片技术，检测层流切应力和震荡切应力条件下 EPCs 及其产生微囊的差异表达 miRs 和差异表达基因;构建不同切应力条件下参与调控 EPCs 功能的 miRs 信号转导网络；建立颈动脉内膜损伤小鼠模型，注射转染目标 miRs inhibitor/mimic的EPCs、转染后 EPCs 分泌的微囊; 检测内膜损伤处的 EPCs 归巢、损伤部位的再内皮化面积和内膜增生等力学特性参数。这一研究旨在探讨扰动流诱导血管内膜损伤的发病机制中，EPCs 及其分泌微囊中 miRs 的作用及其力学生物学机制。

Endothelial progenitor cells (EPCs) can differentiate into mature endothelial cells (ECs), and participate in the reendothelialization of injuried vascular and the angiogenesis of ischemic lesions. How EPC microRNAs (miRs) regulate EPC function and intimal injury repair under shear stress, the mechanism is unclear. In the current project, by using parallel plate flow chamber system, miRs array and mRNA array, the mechanism of EPCs miRs and miRs in EPCs-derived microvesicles influencing EPC proliferation and differentiation is plan to be explored under laminar shear stress and oscillation shear stress. EPCs transfection with miRs inhibitor/mimic and microvesicles derived from EPCs transfection with miRs inhibitor/mimic were injected into carotid artery injury mice via tail vein. EPCs homing, the areas of reendothelialization and the mechanical parameters of neointimal hyperplasia were analysis in order to understand the role of EPCs miRs and miRs in EPCs-derived microvesicles in vascular injury reendothelialization and to investigate the possibilities of the EPCs miRs as a therapeutic target in vascular injury. The purpose of the current project focus on exploring how does the mechanical factors generate the biological effects on the EPC-relative miRs, and to clarify the pathogenesis of vascular remodeling and provide some new insights into mechanotransduction.