miR-302b在糖尿病肾病中抑制高糖诱导上皮间质细胞转化的研究  

MiR-302b suppresses the high-sucrose induced pithelial-mesenchymal transition in diabetic nephropathy

作　　者：张成杰[1] 郑玉明[1] 陈贵言[1] ZHANG Chengjie, ZHENG Yuming, CHEN Guiyan(Department of Emergency, Binzhou Peopleg Hospital, Binzhou 256610, P. R. Chin)

机构地区：[1]滨州市人民医院急诊科,滨州256610

出　　处：《滨州医学院学报》2018年第4期251-254,共4页Journal of Binzhou Medical University

摘　　要：目的糖尿病肾病(DN)是一种糖尿病血管并发症,其发病机制仍然复杂。本研究旨在探讨糖尿病肾病发展过程中,miR-302b在高糖诱导上皮间质细胞转化(EMT)过程中的潜在作用,并揭示其可能的分子机制。方法用高糖(30 mM)处理足细胞与上皮细胞,构建糖尿病肾病模型。用病毒包装法打包miR-302b中的过表达载体,然后转染到足细胞与上皮细胞中。结果在miR-302b的过表达影响下,与上皮间质细胞转化相关的蛋白分子,包括Slug蛋白、Snail蛋白、波形蛋白和纤连蛋白都显著降低,而E-钙黏蛋白、β-连环蛋白、α-连环蛋白显著增加。结论研究结果表明,miR-302b的过表达是通过抑制高糖诱导上皮间质细胞转化过程,从而在糖尿病肾病中起保护作用。Objective Diabetic nephropathy （DN） is a kind of vascular complication for diabetes, and its pathogenesis remains complicate. This study aimed to investigate the potential role of miR-302b in the high-sucrose induced epithelial-mesenehymal transition （EMT） during the development of DN and to reveal its possible molecular mechanism. Methods The podoeytes and epithelial cells were treated with the high-sucrose （ 30 mM ） to construct the DN model. The overexpressed vector of miR-302b was packaged by the virus packaging method and then was transfeeted into the podoeytes and epithelial ceils. Results The EMT-related protein including slug, snail, vimentin and fibroneetin was significantly decreased, whereas E-eadherin, β-eatenin and α-eatenin were significantly in- creased by the overexpression of miR-302b. Conclusion Taken together, our study revealed that the overexpression of miR-302b functioned as a protector in the development of DN by suppressing the high-sucrose induced EMT process.

关 键 词：糠尿病肾病 miR-302b 足细胞 上皮细胞 上皮间质细胞转化 

分 类 号：R587.2[医药卫生—内分泌]