MicroRNA-21 protects from mesangial cell proliferation induced by diabetic nephropathy in db/db mice

被引：285

作者：

Zhang, Zheng ^{[1
,2
]}

Peng, Huimin ^{[1
,2
]}

Chen, Junxia ^{[1
,2
]}

Chen, Xin ^{[3
]}

Han, Fei ^{[1
]}

Xu, Xiaoming ^{[1
]}

He, Xiaoyan ^{[1
]}

Yan, Ning ^{[1
]}

机构：

[1] Chongqing Med Univ, Dept Cell Biol & Med Genet, Chongqing, Peoples R China

[2] Chongqing Med Univ, Mol Med & Canc Res Ctr, Chongqing, Peoples R China

[3] Chongqing Med Univ, Affiliated Hosp 1, Dept Endocrinol, Chongqing, Peoples R China

来源：

FEBS LETTERS | 2009年 / 583卷 / 12期

基金：

中国国家自然科学基金;

关键词：

Diabetic nephropathy; Mesangial cell; MicroRNAs; PTEN phosphohydrolase; SUPPRESSOR GENE; EXPRESSION; PTEN; IDENTIFICATION; HYPERTROPHY; DISEASE; TARGETS; CANCER; MOUSE; SIZE;

D O I：

10.1016/j.febslet.2009.05.021

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

Diabetic nephropathy (DN) is a major diabetic complication. But the initiating molecular events triggering DN are unknown. Recent researches have addressed the role of microRNAs in diabetes and its complications. In this study, we looked for microRNAs expression during early DN, and showed microRNA-21 (miR-21) expression was downregulated in response to early DN in vitro and in vivo. Over-expression of miR-21 inhibited proliferation of mesangial cells and decreased the 24-h urine albumin excretion rate in diabetic db/db mice. Moreover, we identified PTEN as a target of miR-21. We also found PI3 K and p-Akt increased in miR-21 treated mesangial cells and db/db mice. Overall, these studies for the first time provide evidence for the potential role of miR-21 in early DN. (C) 2009 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.

引用

页码：2009 / 2014

页数：6

共 23 条

[1]

Deletion of Pten in mouse brain causes seizures, ataxia and defects in soma size resembling Lhermitte-Duclos disease [J].