期刊论文详细信息
International Journal of Molecular Sciences
MiR542-3p Regulates the Epithelial-Mesenchymal Transition by Directly Targeting BMP7 in NRK52e
Zhicheng Liu2  Yuru Zhou1  Yue Yuan2  Fang Nie2  Rui Peng2  Qianyin Li2  Zhongshi Lyu2  Zhaomin Mao2  Liyuan Huang2  Li Zhou2  Yiman Li2  Jing Hao2  Dongsheng Ni2  Qianni Jin2  Yaoshui Long2  Pan Ju2  Wen Yu2  Jianing Liu2  Yanxia Hu2  Qin Zhou2 
[1] The Seventh Class of 2012 year entry, the Third Clinical College, Chongqing Medical University, Chongqing 400016, China;The Division of Molecular Nephrology and the Creative Training Center for Undergraduates, The M.O.E. Key Laboratory of Laboratory Medical Diagnostics, the College of Laboratory Medicine, Chongqing Medical University, Chongqing 400016, China;
关键词: kidney fibrosis;    miR542-3p;    bone morphogenetic protein 7 (BMP7);    Epithelial-Eesenchymal Transition (EMT);    transforming growth factor beta 1 (TGFβ1);   
DOI  :  10.3390/ijms161126075
来源: mdpi
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【 摘 要 】

Accumulating evidence demonstrated that miRNAs are highly involved in kidney fibrosis and Epithelial-Eesenchymal Transition (EMT), however, the mechanisms of miRNAs in kidney fibrosis are poorly understood. In this work, we identified that miR542-3p could promote EMT through down-regulating bone morphogenetic protein 7 (BMP7) expression by targeting BMP7 3′UTR. Firstly, real-time PCR results showed that miR542-3p was significantly up-regulated in kidney fibrosis in vitro and in vivo. Moreover, Western blot results demonstrated that miR542-3p may promote EMT in the NRK52e cell line. In addition, we confirmed that BMP7, which played a crucial role in anti-kidney fibrosis and suppressed the progression of EMT, was a target of miR542-3p through Dual-Luciferase reporter assay, as did Western blot analysis. The effects of miR542-3p on regulating EMT could also be suppressed by transiently overexpressing BMP7 in NRK52e cells. Taken together, miR542-3p may be a critical mediator of the induction of EMT via directly targeting BMP7.

【 授权许可】

CC BY   
© 2015 by the authors; licensee MDPI, Basel, Switzerland.

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