mi R10通过TGF-β1/SMAD3通路在糖尿病肾脏疾病发病中机制的探讨  

The role of miR10 in the pathogenesis of diabetic kidney disease through TGF-β1/Smad 3 pathway

作　　者：王怡丽 周阳[1] 康嘉懿 袁紫东 王秋月[1] WANG Yi-li;ZHOU Yang;KANG Jia-yi;YUAN Zi-dong;WANG Qiu-yue(Department of Endocrinology and metabolism,the First Hospital of China Medical University,Shenyang 110001,China)

机构地区：[1]中国医科大学附属第一医院内分泌与代谢病,辽宁沈阳110001

出　　处：《解剖科学进展》2020年第6期630-633,共4页Progress of Anatomical Sciences

基　　金：辽宁省高等学校“高端人才队伍建设工程”项目([2014]187)。

摘　　要：目的探讨miR10在体外高糖培养条件下对大鼠肾小球系膜细胞诱导纤维化中的作用与机制。方法使用高糖培养模拟糖尿病环境,用qRT-PCR检测细胞中miR10的变化,Western blot检测TGF-β1、SMAD3、CTGF的蛋白表达。siRNA转染抑制高糖培养下大鼠肾小球系膜细胞中miR10a的表达水平后,Western blot方法检测TGF-β1、SMAD3、CTGF的表达变化。结果与正常糖培养组相比,高糖组大鼠肾小球系膜细胞MIR10、TGF-β1、SMAD3、CTGF明显增加(P<0.05)。抑制细胞内miR10的表达水平后,高糖培养组TGF-β1,SMAD3、CTGF蛋白表达明显下降(P<0.05),正常糖组TGF-β1,SMAD3、CTGF无明显变化(P>0.05)。结论高糖环境下,miR10可通过调控TGF-β1/SMAD3信号途径抑制RMCs纤维化。Objective To explore the role and mechanism of MIR10 in inducing fibrosis in rat mesangial cells under high glucose culture conditions in vitro.Methods High glucose culture was used to simulate the diabetic environment,qRT-PCR was used to detect the changes of MIR10 in the cells,and Western blot was used to detect the protein expression of TGF-β1,SMAD3 and CTGF.Subsequently,it inhibited MIR10 in rat glomerular mesangial cells under high glucose culture,and detected TGF-β1,SMAD3,CTGF by Western blot.Results Compared with the normal sugar culture group,the high sugar group mice kidney glomerular cell miR10,TGF-beta 1,SMAD3,CTGF significantly increased(P<0.05).After inhibiting the expression of miR10 in the cells,the expression of the high sugar culture group TGF-beta 1,SMAD3,CTGF protein expression decreased significantly(P<0.05),the normal sugar group TGF-beta1,SMAD3.Conclusion miR10 can inhibit RMCS fibrosis by regulating TGF-β1/Smad3 signaling pathway in high glucose environment.

关 键 词：糖尿病肾脏疾病 微小RNA miR10 转移生长因子-Β1 纤维化 

分 类 号：R587.2[医药卫生—内分泌]