miR-221/222表达在心肌缺血动物模型内皮祖细胞心肌归巢促血管生成中的调节机制研究

目前诱导新生血管形成挽救濒死心肌已成为治疗严重心肌缺血的一种新策略。microRNA是一种非编码RNA，参与基因的转录后调控，研究证实miR-221/222在缺血心肌血管生成的发生发展中可能起重要调控作用。血管内皮祖细胞(EPCs)是血管内皮的前体细胞，在缺血心肌中可以诱导分化为血管内皮细胞，并形成新生血管，血管内皮生长因子（VEGF）是此过程中最主要的促进因子。课题组在前期研究中发现miR-221/222与VEGF表达水平负相关，且皆与侧枝循环建立密切相关，以此为基础，本课题将探讨miR-221/222在循环内皮祖细胞中对VEGF的调控机制，以及在此调控基础上，miR-221/222对内皮祖细胞向内皮细胞分化及成血管能力的调节作用。进而，探讨miR-221/222作为缺血心肌内皮祖细胞心肌归巢促血管生成干预靶点的可能性。

Pro-angiogenesis has became a new strategy to save the starving myocardial in treating severe myocardial ischemia. MicroRNA is a kind of non-coding RNA and participates in the regulation of post-transcription. Previous studies have proved that miR-221/222 play an important role in the development of angiogenesis of ischemic myocardial. Endothelial progenitor cells (EPCs) are the progenitor cells of vascular endothelium, which can differentiate to vacular endothelial cells (ECs) and form neovascularization. Vascular endothelial growth factor (VEGF) is the most important promoter in this process. In previous studies, we have proved that the expression of miR-221/222 is negatively related with the level of VEGF, and is closely related with the collateral. This study will discuss the mechanism of miR-221/222 in regulating the expression of VEGF in EPCs and the role of miR-221/222 in regulating the differentiation of EPCs to ECs and the ability of angiogenesis. And through the study above, we will discuss the possibility of miR-221/222 as a treating target in EPCs homing and proangiogenesis in ischemic myocardial.