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Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration

Huang, Wei, Feng, Yuliang, Liang, Jialiang, Yu, Hao, Wang, Cheng, Wang, Boyu, Wang, Mingyang, Jiang, Lin, Meng, Wei, Cai, Wenfeng, Medvedovic, Mario, Chen, Jenny, Paul, Christian, Davidson, W. Sean, Sadayappan, Sakthivel, Stambrook, Peter J., Yu, Xi-Yong, Wang, Yigang·2018·Nature Communications
DOI 10.1038/s41467-018-03019-zPMC PMC5816015
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Abstract

The goal of replenishing the cardiomyocyte (CM) population using regenerative therapies following myocardial infarction (MI) is hampered by the limited regeneration capacity of adult CMs, partially due to their withdrawal from the cell cycle. Here, we show that microRNA-128 (miR-128) is upregulated in CMs during the postnatal switch from proliferation to terminal differentiation. In neonatal mice, cardiac-specific overexpression of miR-128 impairs CM proliferation and cardiac function, while miR-128 deletion extends proliferation of postnatal CMs by enhancing expression of the chromatin modifier SUZ12, which suppresses p27 (cyclin-dependent kinase inhibitor) expression and activates the positive cell cycle regulators Cyclin E and CDK2. Furthermore, deletion of miR-128 promotes cell cycle re-entry of adult CMs, thereby reducing the levels of fibrosis, and attenuating cardiac dysfunction in response to MI. These results suggest that miR-128 serves as a critical regulator of endogenous CM proliferation, and might be a novel therapeutic target for heart repair.

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Metadata

Authors
Huang, W., Feng, Y., Liang, J., Yu, H., Wang, C., Wang, B., Wang, M., Jiang, L., Meng, W., Cai, W., Medvedovic, M., Chen, J., Paul, C., Davidson, W. S., Sadayappan, S., Stambrook, P. J., Yu, X.-Y., & Wang, Y.
ORCID
Venue
Nature Communications
Publisher
Springer Science and Business Media LLC
Published
2018-02-16
Volume
9
Issue
1
ISSN
2041-1723
DOI
10.1038/s41467-018-03019-z
PMC
PMC5816015
Cited by
139
References
7
Language
en
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