心肌梗死是由冠状动脉病变引起血供减少或中断，使心肌严重持久缺血所致的坏死。细胞凋亡是缺血所致心肌细胞死亡的途径之一。近年发现，MicroRNA (miRNA)-1与miRNA-133是在成熟心肌中特异性高表达的miRNA，在心肌梗死及细胞凋亡中发挥着重要的调节作用。我们在前期工作中观察到，在大鼠急性心肌梗死模型下，人羊膜上皮细胞分化为心肌样细胞、减少梗死心肌面积、改善心功能。本项目拟通过建立在体和体外大鼠急性心肌梗死模型，观察人羊膜上皮细胞移植对急性心肌梗死心肌细胞凋亡的影响，人羊膜上皮细胞移植对miRNA-1与miRNA-133表达的影响，人羊膜上皮细胞抑制心肌细胞凋亡的靶点基因、信号转导机制，以论证人羊膜上皮细胞调控miRNA-1与miRNA-133的表达，抑制心肌细胞凋亡，保护心肌的假说，探讨其抗细胞凋亡的细胞分子机制，为人羊膜上皮细胞在心肌梗死干细胞治疗应用上提供坚实的理论依据。

Myocardial infarction (MI) refers to the myocardial necrosis resulted from serious and persistent ischemia which occurs when coronary artery lesion causes reduction or interruption of blood supply. Cell apoptosis is one of the ways that ischemia causes myocardial cell death. Recent study found that MicroRNA (miRNA)-1 and miRNA-133 specifically highly expressed miRNA in the mature myocardial tissues, which play an important regulatory role in MI and cell apoptosis. We observed in our previous work that in the rat model of acute MI, human amniotic epithelial cells (h-AECs) differentiated into cardiomyocyte-like cells in vivo, reduced the infarct area, and improved cardiac function. This project intends to observe the influences of h-AECs transplantation on myocardial cell apoptosis and on expressions of miRNA-1 and miRNA-133 through the acute MI model in rats in vivo and in vitro, and to explore the target gene and signal transduction mechanism for h-AECs to inhibit myocardial cell apoptosis, in order to demonstrate the hypothesis that h-AECs inhibit myocardial cell apoptosis and protect myocardium by regulating the expressions of miRNA-1 and miRNA-133, discuss the molecular mechanism of its anti-apoptosis role, and provide a solid theoretical basis for application of h-AECs in stem cell therapy for MI.