High glucose down-regulates miR-29a to increase collagen IV production in HK-2 cells

被引：183
作者：
Du, Bin [1 ]
Ma, Li-Ming [1 ]
Huang, Mian-Bo [1 ]
Zhou, Hui [1 ]
Huang, Hui-Lin [1 ]
Shao, Peng [1 ]
Chen, Yue-Qin [1 ]
Qu, Liang-Hu [1 ]
机构：
[1] Sun Yat Sen Univ, Biotechnol Res Ctr, State Key Lab Biocontrol, Key Lab Gene Engn,Minist Educ, Guangzhou 510275, Guangdong, Peoples R China
来源：
FEBS LETTERS | 2010年 / 584卷 / 04期
基金：
中国国家自然科学基金;
关键词：
miR-29a; Collagen IV; High glucose; TGF-beta; 1; HK-2; cell; DIABETIC KIDNEY-DISEASE; PROXIMAL TUBULAR CELLS; MICRORNAS; BETA; FIBRONECTIN; EXPRESSION; EXPOSURE;
D O I：
10.1016/j.febslet.2009.12.053
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Deposition of collagen IV in proximal tubule cells (PTCs) plays an important role during diabetic nephropathy, but the mechanism underlying excessive production of collagen IV remains poorly understood. In this study, we examined the miRNA profile of HK-2 cells and found that high glucose/TGF-beta 1 induced significant down-regulation of miR-29a. We then showed that miR-29a negatively regulated collagen IV by directly targeting the 3'UTRs of col4a1 and col4a2. These results suggest that miR-29a acts as a repressor to fine-tune collagen expression and that the reduction of miR-29a caused by high glucose may increase the risk of excess collagen deposition in PTCs. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.
引用
收藏
页码：811 / 816
页数：6
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