血管成形术及经皮冠状动脉介入治疗术后再狭窄是心血管疾病国内外研究的重要方向,新生内膜增生是再狭窄等心血管疾病共同的病理特征。因此研究新生内膜形成的原因、细胞组成及功能对于防治此类疾病有着重要意义。故本课题拟在前期工作的基础上，以大鼠及基因敲除小鼠损伤血管为研究对象，体内和体外实验采用实时定量PCR、WB、细胞转染、FRET技术、酶联免疫吸附实验，MSC和VSMC的分离和培养,细胞迁移实验等技术检测血管损伤后局部微环境及MSC和VSMC中MMP-14和TGF-β1信号转导通路蛋白的表达情况及相互作用,研究MMP-14和TGF-β1在动员和招募聚集骨髓腔的MSC到血管损伤部位,促进其向VSMC分化及中膜VSMC向内膜的迁移，导致血管新生内膜形成整个过程中的作用。进而探讨血管损伤后新生内膜形成的机制并探索针对该通路的有效干预手段，旨在为预防和治疗冠状动脉介入治疗术后冠脉再狭窄提供新思路。

Postoperative restenosis of angioplasty or percutaneous coronary artery intervention treatment is the important issue in cardiovascular disease. Neointimal hyperplasia of restenosis is a common characteristics of pathological changes in cardiovascular diseases. To explore the cause of neointimal formation, cell composition and function are important for prevention and treatment of these diseases. Based on previous work, real time quantitative PCR, WB and ELISA have been applied to detect the expression of MMP-14 and TGF-β1. In vitro, MSC and VSMC isolated from S-D rat. The MMP-14 biosensor were transfected into different types of cells. Fluorescence resonance energy transfer（FRET）imagine was utilized to observe the dynamic changes between MMP-14 and TGF-β1 in live cells. In vivo, artery injury animal models are built in rats and gene knockout mice, then to learn the interaction and function of MMP-14 and TGF-β1 in neointimal formation. To study the possible mechanism of MMP-14 and TGF-β1 in mobilizing and recruiting bone marrow MSC to the area of artery injury, promote to VSMC differentiation and the VSMC in tunica media migration to the neointima. And then discuss the mechanism of effective interventions for restenosis after coronary interventional treatment.