肌醇促进鱼肠细胞增殖与信号分子E2F4的关系研究

鱼类肠道是营养物质消化吸收的重要器官，但易引起氧化损伤破坏其结构，导致功能异常。肠上皮细胞是鱼肠主要的功能细胞，肌醇能通过提高鱼肠细胞增殖来维持肠道结构完整性和功能正常，但作用机制尚不清楚。E2F4是调控人肠细胞增殖的关键信号分子，但其在鱼肠中是否有相似的作用未见报道。因此，本项目拟率先研究信号分子E2F4及相关因子cyclin A、B、D1、E在鲤鱼肠组织中是否存在及表达规律，并采用本课题组研究建立的体外培养细胞模型，利用基因沉默技术研究信号分子E2F4是否参与鱼肠细胞增殖调控；进一步用肌醇处理，考察肌醇是否通过调控E2F4及其下游靶基因cyclin来促进鱼肠细胞增殖。通过本项目的实施首次探索了信号分子E2F4在鱼肠组织中是否存在及其表达规律；率先研究其是否参与鱼肠细胞增殖调控；率先研究肌醇是否通过信号分子E2F4调控鱼肠细胞增殖及作用方式，为探索肌醇促进鱼类生长的机制提供理论支持。

Intestine is important to nutrient digestion and absorption, especially to stomachless fish, but it is susceptible to oxidative injury. Myo-inositol (MI) can increase the proliferation of enterocytes, and thus maintain intestinal integrity and function. E2F4 is the transcript factor known that regulates the proliferation of human enterocytes. However, whether a similar regulatory role of E2F4 also plays in fish intestine has not yet been studied. Therefore, this project will investigate that whether signaling molecule E2F4 as well as cyclin A, B, D1 and E exist in the intestine and the expression pattern of these genes. Next, using in vitro cell model established by our laboratory, we will study whether signal molecule E2F4 involves in the regulation of the fish enterocyte proliferation by using gene silencing technology. Furthermore, treated fish enterocytes with MI, and then examine the relationship between MI-improved the proliferation of enterocytes and the E2F4 signaling pathways, and also investigate the potential action pathway through cyclin. Summarily, this project will reveal the relationship between MI-promoted the proliferation of enterocytes and the E2F4 signaling, which may provide some theoretical supports to the mechanism of MI-induced fish growth.