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Nucleic Acids Research Advance Access published online on March 19, 2008
Nucleic Acids Research, doi:10.1093/nar/gkn032
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© 2008 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Molecular Biology

Transforming growth factor-β-regulated miR-24 promotes skeletal muscle differentiation

Qiang Sun1, Yan Zhang1, Guang Yang2, Xiaoping Chen3, Yingai Zhang1, Guojun Cao2, Jian Wang1, Yanxun Sun1, Peng Zhang3, Ming Fan2, Ningsheng Shao2 and Xiao Yang1,*

1State Key Laboratory of Proteomics, Genetic Laboratory of Development and Diseases, Institute of Biotechnology, 20 Dongdajie, Beijing 100071, 2Institute of Basic Medical Sciences, 27 Taiping Road, Beijing 100850 and 3China Astronaut Research and Training Center, Yuanmingyuan West Road, Beijing 100094, P. R. China

*To whom correspondence should be addressed. Tel: +86 10 63895937; Fax: +86 10 63895937; Email: yangx{at}nic.bmi.ac.cn Correspondence may also be addressed to Ningsheng Shao. Tel: +86 10 68163140; Fax: +86 10 68163140; Email: shaons{at}yahoo.com

Received December 29, 2007. Accepted January 19, 2008.

MicroRNAs (miRNAs) have recently been proposed as a versatile class of molecules involved in regulation of a variety of biological processes. However, the role of miRNAs in TGF-β-regulated biological processes is poorly addressed. In this study, we found that miR-24 was upregulated during myoblast differentiation and could be inhibited by TGF-β1. Using both a reporter assay and Northern blot analysis, we showed that TGF-β1 repressed miR-24 transcription which was dependent on the presence of Smad3 and a Smads binding site in the promoter region of miR-24. TGF-β1 was unable to inhibit miR-24 expression in Smad3-deficient myoblasts, which exhibited accelerated myogenesis. Knockdown of miR-24 led to reduced expression of myogenic differentiation markers in C2C12 cells, while ectopic expression of miR-24 enhanced differentiation, and partially rescued inhibited myogenesis by TGF-β1. This is the first study demonstrating a critical role for miRNAs in modulating TGF-β-dependent inhibition of myogenesis, and provides a novel mechanism of the genetic regulation of TGF-β signaling during skeletal muscle differentiation.

The authors wish it to be known that, in their opinion, the first three authors should be regarded as joint First Authors.


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