骨髓间充质干细胞（MSC）促血管新生是治疗心肌梗死的新策略，但梗死区周边血管内皮细胞的病理状态严重影响MSC的疗效，找到缺血缺氧微环境调控MSC增殖及分化的关键因子是提高MSC移植效果的重要策略。前期实验及文献证实，基质衍生因子-1（SDF-1）及其受体CXCR4是调节血管新生的中枢性环节，而PGC-lα影响内皮细胞的抗氧化、增殖、迁移，是调节血管新生的重要转录调节因子。但是，心梗中内皮细胞PGC-lα的改变是否作用于SDF-1/CXCR4轴，影响MSC的增殖及内皮分化,目前仍不清楚。 本研究拟通过基因谱系示踪技术,观察β-半乳糖苷酶基因z(LacZ) 阳性PGC-lα敲除的内皮细胞与绿色荧光蛋白(GFP)标记的CXCR4阳性MSC之间的相互作用及下游PI3K信号通路的改变，探讨缺血、缺氧环境中内皮细胞PGC-lα活性的改变对MSC促血管新生的作用及其机制，为心梗的干细胞治疗提供新思路。

The potential of bone marrow mesenchymal stem cells (MSC) to enhance neoangiogenesis provides a novel therapeutic strategy for myocardial infarction. However, the pathological state of blood vessels in the peri-infarct area affects local blood supply, which may consequently reduce the efficacy of MSC transplantation therapy. Therefore, identification of the key factors which promote angiogenesis is of great significance in MSC therapy. Our previous studies and literatures confirm that the stromal-derived factor-1 (SDF-1) and its receptor CXC chemokine receptor type 4 (CXCR4) are the major factors in mediating angiogenesis, and that the peroxisome-proliferator-activated receptor γ-coactivator-lα (PGC-lα) is an important transcriptional regulator of angiogenesis. However, the mechanisms that underlie the regulative effects of endothelial cell PGC-lα on the SDF-1/CXCR4 axis remain elusive. In this project, we proposed to investigate the interaction between LacZ positive PGC-1α knockout endothelial cell and GFP tagged CXCR4 positive MSC, and the effects of its downstream PI3K signaling pathway. In this way, we will elucidate the role of endothelial cell PGC-1α in the MSC mediated angiogenesis. This project will provide a new stem cell-based therapeutic avenue for myocardial infarction.