c-kit是心肌干细胞（CSCs）特异性表面标志，心梗后c-kit表达增高，对损伤心肌有修复作用。我们的前期试验显示基质细胞衍生因子-1（SDF-1）能上调CSCs表面c-kit表达；c-kit+与c-kit-CSCs存在明显甲基化差异。但机制不明。本课题拟①将DNMT质粒及DNMT-siRNA质粒转染CSCs，观察c-kit、DNA甲基转移酶（DNMT）表达②SDF-1及PI3K/Akt信号通路特异性抑制剂LY294002干预CSCs，观察DNMT、磷酸化Akt表达③将SDF-1及LY294002干预的CSCs移植入心梗模型大鼠心肌内，观察心梗面积、心功能及c-kit、DNMT表达。论证PI3K/AKT信号通路激活致DNMT减少，使c-kit基因低甲基化，c-kit表达增加，增强CSCs迁移、增殖潜能。本研究探索c-kit基因表达对CSCs影响及分子机制，为缺血性心脏病的治疗提供新靶点。

C-kit is a specific surface markers of CSCs . In myocardium after AMI,the density of c-kit+CSCs and c-kit expression are increased significantly,which is a good repair effect to the injury of the myocardium. Our preliminary experiments show SDF-1 can increase the surface expression of c-kit,and the methylation differences between c-kit-CSCs and c-kit+CSCs are significant. However,its precise mechanism is unknown. This project intends to①transfecting plasmid DNMT and DNMT-siRNA plasmid into CSCs, observation on c-kit,DNMT expression and so on. ②CSCs is intervented by SDF-1 ,and ade in LY294002,which is specific inhibitor of PI3K / Akt signaling pathway,observation on c-kit,DNMT, phosphorylated Akt expression,and so on. ③CSCs which is intervented by SDF-1 and LY294002 are transplanted into the c-kit gene knockout models of AMI rat myocardium,observation on myocardial infarct size, heart function and c-kit, DNMT expression. Demonstration of PI3K / AKT signaling pathway activation results in DNMT reduction,c-kit gene hypomethylation, and the expression of c-kit increased, then enhance migration ability,proliferation ability of CSCs,and the regeneration and repair of cardiac injury potential. This study perspective to explore the effect of c-kit to CSCs and the related molecular mechanism, for the treatment of ischemic heart disease with a new target.