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

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 ca...

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Bibliographic Details
Published in:International journal of molecular sciences 2016-06, Vol.17 (6), p.848-848
Main Authors: Liu, Jing-Jing, Zhao, Cui-Mei, Li, Zhi-Gang, Wang, Yu-Mei, Miao, Wei, Wu, Xiu-Juan, Wang, Wen-Jing, Liu, Chang, Wang, Duo, Wang, Kang, Li, Li, Peng, Lu-Ying
Format: Article
Language:English
Subjects:
Animals
cardiomyocyte
Cardiomyocytes
Cells, Cultured
Constriction, Pathologic - chemically induced
Constriction, Pathologic - genetics
Disease Models, Animal
Down-Regulation
Gene expression
Gene Expression Regulation - drug effects
Heart failure
hypertrophy
Isoproterenol - adverse effects
Mice
MicroRNAs
MicroRNAs - genetics
miR-218
Myocytes, Cardiac - cytology
Myocytes, Cardiac - drug effects
Myocytes, Cardiac - pathology
Rats
Repressor Proteins - genetics
REST
Signal Transduction
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Summary: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.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms17060848