内皮细胞受损及功能障碍是肺动脉高压(PAH)的始动环节，也是肺血管损伤后 不良修复反应的主因之一。内皮祖细胞(EPCs)移植是治疗血管损伤的重要方法，但EPCs在受体内存活不足且尚无向损伤肺血管优势分布的有效措施，限制了EPCs移植治疗肺血管损伤应用及疗效。本项目以大鼠缺氧性PAH为模型，用液体闪烁计数、MRI示踪、定量PCR等方法获得移植的EPCs在大鼠体内的细胞定位和动态分布完整资料。充分动员大鼠自体EPCs，体外培养并分离鉴定，构建c-met的腺病毒表达载体，转染至EPCs，通过静脉回输同一鼠体内，利用肺血管损伤时血清及肺血管损伤部位肝细胞生长因子(HGF)含量增加的特点，观察 HGF/c-met轴促进自身EPCs及移植EPCs存活并向PAH损伤肺血管靶向分布修复肺血管损伤的影响及其可能机制，从整体-血管环-细胞三个层次寻求一种更为高效、特异的EPCs移植防治肺动脉高压的治疗策略。

Endothelial cell injury and dysfunction is not only the initial step for the pulmonary arterial hypertension(PAH), also one of principal cause of adverse repair actions of pulmonary vascular injury. Transplantations of endothelial progenitor cell(EPCs) is the important therapy to the vascular injury, but deficiency of EPCs in recipients and no effective measures guiding to dominant distribution of pulmonary vascular injury restrict the curative effect and clinical implication of the treatment by transplantation of EPCs. Establishing the rat models with hypoxic PAH, with the methods of Liquid Scintillation Counting, MRI tracer, quantitative PCR, we collected the complete data of Cellular Localization and normal distribution of the transplanted EPCs. This program activated adequately EPCs in rats, with Isolation and Identification after cultivated in vitro, and constructed the adenovirus expression vector of c-met to transfect into EPCs in rats, then infused to the same rat. With the characteristic of increase of serum and hepatocyte growth factor (HGF) content in location of pulmonary vascular injury, we observe the influence and mechanism of HGF-c-met axes promotion the survival of transplanted EPCs and targeting distribution of PAH induced pulmonary vascular injury to repair, searching out further specificity and efficiency strategies for the treatment of PAH with EPCs transplantation to provide a new target of the prevention and cure of PAH. KEY WORDS: hypoxic pulmonary arterial hypertension; pulmonary vascular remodeling; HGF; dominant distribution