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Int. J. Mol. Sci. 2016, 17(6), 848;

miR-218 Involvement in Cardiomyocyte Hypertrophy Is Likely through Targeting REST

Key Laboratory of Arrhythmias, Ministry of Education, Tongji University School of Medicine, Shanghai 200092, China
Research Center for Translational Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200120, China
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: Martin Pichler
Received: 23 April 2016 / Revised: 10 May 2016 / Accepted: 25 May 2016 / Published: 31 May 2016
(This article belongs to the Collection Regulation by Non-Coding RNAs)
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MicroRNAs (miRNAs) have been identified as key players in cardiomyocyte hypertrophy, which is associated with significant risks of heart failure. However, many microRNAs are still not recognized for their functions in pathophysiological processes. In this study, we evaluated effects of miR-218 in cardiomyocyte hypertrophy using both in vitro and in vivo models. We found that miR-218 was evidently downregulated in a transverse aortic constriction (TAC) mouse model. Overexpression of miR-218 is sufficient to reduce hypertrophy, whereas the suppression of miR-218 aggravates hypertrophy in primary cardiomyocytes induced by isoprenaline (ISO). In addition, we identified RE1-silencing transcription factor (REST) as a novel target of miR-218; it negatively regulated the expression of REST in hypertrophic cardiomyocytes and the TAC model. These results showed that miR-218 plays a crucial role in cardiomyocyte hypertrophy, likely via targeting REST, suggesting a potential candidate target for interfering hypertrophy. View Full-Text
Keywords: miR-218; cardiomyocyte; hypertrophy; REST miR-218; cardiomyocyte; hypertrophy; REST

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Liu, J.-J.; Zhao, C.-M.; Li, Z.-G.; Wang, Y.-M.; Miao, W.; Wu, X.-J.; Wang, W.-J.; Liu, C.; Wang, D.; Wang, K.; Li, L.; Peng, L.-Y. miR-218 Involvement in Cardiomyocyte Hypertrophy Is Likely through Targeting REST. Int. J. Mol. Sci. 2016, 17, 848.

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