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Int. J. Mol. Sci. 2015, 16(10), 24032-24047; doi:10.3390/ijms161024032

MiR-30a Inhibits the Epithelial—Mesenchymal Transition of Podocytes through Downregulation of NFATc3

1
The Divsion 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
2
The College of Laboratory Medicine, Chongqing Medical University, Chongqing 400016, China
3
The First Hospital of Xi’an, Xi’an 710002, China
4
Key Laboratory for Regenerative Medicine, Ministry of Education, School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China
5
Core Facility of Experiments Training, Chongqing Medical University, Chongqing 400016, China
These authors contributed equally to this work.
*
Author to whom correspondence should be addressed.
Academic Editor: Y-h. Taguchi
Received: 8 August 2015 / Revised: 31 August 2015 / Accepted: 29 September 2015 / Published: 12 October 2015
(This article belongs to the Special Issue MicroRNA Regulation)
View Full-Text   |   Download PDF [3009 KB, uploaded 12 October 2015]   |  

Abstract

MicroRNAs (miRNAs) possess an important regulating effect among numerous renal diseases, while their functions in the process of epithelial-to-mesenchymal transition (EMT) after podocyte injury remain unclear. The purpose of our study is to identify the potential functions of miR-30a in EMT of podocytes and explore the underlying mechanisms of miR-30a in the impaired podocytes. The results revealed that downregulation of miR-30a in podocyte injury animal models and patients, highly induced the mesenchymal markers of EMT including Collagen I, Fibronectin and Snail. Furthermore, overexpression of miR-30a enhances epithelial markers (E-cadherin) but diminished mesenchymal markers (Collagen I, Fibronectin and Snail) in podocytes. In addition, we established miR-30a target NFATc3, an important transcription factor of Non-canonical Wnt signaling pathway. More importantly, our findings demonstrated that the augmentation of miR-30a level in podocytes inhibits the nuclear translocation of NFATc3 to protect cytoskeleton disorder or rearrangement. In summary, we uncovered the protective function of miR30a targeting NFATc3 in the regulation of podocyte injury response to EMT. View Full-Text
Keywords: microRNA-30a (miR-30a); podocyte; epithelial-to-mesenchymal transition (EMT); nuclear factor of activated T cells 3 (NFATc3) microRNA-30a (miR-30a); podocyte; epithelial-to-mesenchymal transition (EMT); nuclear factor of activated T cells 3 (NFATc3)
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Peng, R.; Zhou, L.; Zhou, Y.; Zhao, Y.; Li, Q.; Ni, D.; Hu, Y.; Long, Y.; Liu, J.; Lyu, Z.; Mao, Z.; Yuan, Y.; Huang, L.; Zhao, H.; Li, G.; Zhou, Q. MiR-30a Inhibits the Epithelial—Mesenchymal Transition of Podocytes through Downregulation of NFATc3. Int. J. Mol. Sci. 2015, 16, 24032-24047.

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