糖尿病性勃起功能障碍(DED)的核心发病机制是血管内皮功能障碍，而PI3K/Akt通路异常是其发生血管内皮功能障碍的重要机制。我们的前期研究发现bFGF基因可通过PI3K/Akt通路调控尿源干细胞(USCs)的增殖、分化、旁分泌。进一步实验发现使用USCs/bFGF能显著改善DED大鼠的阴茎海绵窦内皮细胞功能及勃起功能，但作用机制未明。因此本项目拟通过过表达和基因沉默、基因芯片及反向蛋白芯片等技术进一步分析b FGF基因如何通过PI3K/Akt通路调控USCs的增殖、分化、旁分泌，并将USCs/bFGF移植入DED大鼠阴茎海绵体，综合分析bFGF基因是否及如何调控移植后的USCs及局部微环境中异常的PI3K/Akt通路, 以纠正DED大鼠的阴茎海绵窦内皮功能及勃起功能，旨在探索bFGF基因调控USCs治疗DED的作用及机制，为确立USCs/bFGF作为DED的治疗新方法提供科学依据。

The core pathologic mechanism of diabetic erectile dysfunction is endothelial dysfunction and it may result from the abnormal PI3K/Akt pathway. Our previous studies demonstrated bFGF gene could promote proliferation, differentiation, paracrine secretion of urine derived stem cells(USCs) in vitro and it was regulated by PI3K/Akt pathway. Furthermore, the USCs expressing bFGF(USCs/bFGF) could recover the erectile function and endothelial function of DED rats when they were implanted into their penis. However, the mechanisms still remain unclear. Therefore, we are planning to analyze how do the bFGF gene regulates the proliferation, differentiation and paracrine secretion of USCs through PI3K/Akt pathway in vitro by the gene over expression, gene silence, gene microarray, RPPA analysis et al. Moreover, we will transplant USCs/bFGF into the DED rats’ penis to study if the bFGF regulate the USCs and recover the local abnormal PI3K/Akt pathway to restore their impaired erectile dysfunction and endothelial dysfunction and its mechanisms. The purpose of this proposal is to study the effects and its mechanisms of USCs on DED and to provide scientific evidence for the establishment of USCs/bFGF as a new therapy for DED in future.