In Vitro Evidence Suggests That miR-133a-mediated Regulation of Uncoupling Protein 2 (UCP2) Is an Indispensable Step in Myogenic Differentiation

被引：88

作者：

Chen, Xi ^{[1
]}

Wang, Kehui ^{[1
]}

Chen, Jiangning ^{[1
]}

Guo, Jigang ^{[1
]}

Yin, Yuan ^{[1
]}

Cai, Xing ^{[1
]}

Guo, Xing ^{[1
]}

Wang, Guoqiang ^{[1
]}

Yang, Rong ^{[1
]}

Zhu, Lingyun ^{[1
]}

Zhang, Yan ^{[1
]}

Wang, Jin ^{[1
]}

Xiang, Yang ^{[1
]}

Weng, Chunyue ^{[1
]}

Zen, Ke ^{[1
]}

Zhang, Junfeng ^{[1
]}

Zhang, Chen-Yu ^{[1
]}

机构：

[1] Nanjing Univ, Sch Life Sci, Jiangsu Diabet Ctr, State Key Lab Pharmaceut Biotechnol, Nanjing 210093, Jiangsu, Peoples R China

来源：

JOURNAL OF BIOLOGICAL CHEMISTRY | 2009年 / 284卷 / 08期

基金：

中国国家自然科学基金;

关键词：

CARDIAC-HYPERTROPHY; ENERGY-METABOLISM; REDOX-REGULATION; MUSCLE-CELLS; MICRORNAS; TRANSCRIPTION; EXPRESSION; HEART; MODULATE; STRESS;

D O I：

10.1074/jbc.M807523200

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：

UCP2 and UCP3, two novel uncoupling proteins, are important regulators of energy expenditure and thermogenesis in various organisms. The striking disparity between UCP2 mRNA and protein levels in muscle tissues prompted initial speculation that microRNAs are implicated in the regulatory pathway of UCP2. We found, for the first time, that the repression of UCP2 expression in cardiac and skeletal muscle resulted from its targeting by a muscle-specific microRNA, miR-133a. Moreover, our findings illustrate a novel function of UCP2 as a brake for muscle development. We also show that MyoD can remove the braking role of UCP2 via direct up-regulation of miR-133a during myogenic differentiation. Taken together, our current work delineates a novel regulatory network employing MyoD, microRNA, and uncoupling proteins to fine-tune the balance between muscle differentiation and proliferation during myogenesis.

引用

页码：5362 / 5369

页数：8

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