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Int. J. Mol. Sci. 2015, 16(3), 5420-5433; doi:10.3390/ijms16035420

MiR-25 Protects Cardiomyocytes against Oxidative Damage by Targeting the Mitochondrial Calcium Uniporter

1,2,3,4,†
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1,4,†
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1,4,†
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1,4
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1,4
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1,4
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1,2,3
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1,2,3,* and 1,2,3,4,5,*
1
Key Laboratory of Arrhythmias of the Ministry of Education of China, East Hospital, Tongji University School of Medicine, Shanghai 200120, China
2
Research Center for Translational Medicine, East Hospital, Tongji University School of Medicine, Shanghai 200120, China
3
Institute of Medical Genetics, Tongji University, Shanghai 200092, China
4
Department of Cardiology, East Hospital, Tongji University School of Medicine, Shanghai 200120, China
5
Department of Pathology and Pathophysiology, Tongji University School of Medicine, Shanghai 200092, China
These authors contributed equally to this work.
*
Authors to whom correspondence should be addressed.
Academic Editor: William Chi-shing Cho
Received: 4 January 2015 / Revised: 4 January 2015 / Accepted: 27 February 2015 / Published: 10 March 2015
(This article belongs to the Special Issue Pathogenesis of Cardiac Arrhythmias and Heart Failure)
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Abstract

MicroRNAs (miRNAs) are a class of small non-coding RNAs, whose expression levels vary in different cell types and tissues. Emerging evidence indicates that tissue-specific and -enriched miRNAs are closely associated with cellular development and stress responses in their tissues. MiR-25 has been documented to be abundant in cardiomyocytes, but its function in the heart remains unknown. Here, we report that miR-25 can protect cardiomyocytes against oxidative damage by down-regulating mitochondrial calcium uniporter (MCU). MiR-25 was markedly elevated in response to oxidative stimulation in cardiomyocytes. Further overexpression of miR-25 protected cardiomyocytes against oxidative damage by inactivating the mitochondrial apoptosis pathway. MCU was identified as a potential target of miR-25 by bioinformatical analysis. MCU mRNA level was reversely correlated with miR-25 under the exposure of H2O2, and MCU protein level was largely decreased by miR-25 overexpression. The luciferase reporter assay confirmed that miR-25 bound directly to the 3' untranslated region (UTR) of MCU mRNA. MiR-25 significantly decreased H2O2-induced elevation of mitochondrial Ca2+ concentration, which is likely to be the result of decreased activity of MCU. We conclude that miR-25 targets MCU to protect cardiomyocytes against oxidative damages. This finding provides novel insights into the involvement of miRNAs in oxidative stress in cardiomyocytes. View Full-Text
Keywords: cardiomyocytes; miR-25; mitochondrial calcium uniporter; oxidative stress cardiomyocytes; miR-25; mitochondrial calcium uniporter; oxidative stress
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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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MDPI and ACS Style

Pan, L.; Huang, B.-J.; Ma, X.-E.; Wang, S.-Y.; Feng, J.; Lv, F.; Liu, Y.; Liu, Y.; Li, C.-M.; Liang, D.-D.; Li, J.; Xu, L.; Chen, Y.-H. MiR-25 Protects Cardiomyocytes against Oxidative Damage by Targeting the Mitochondrial Calcium Uniporter. Int. J. Mol. Sci. 2015, 16, 5420-5433.

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