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miRNA-204 drives cardiomyocyte proliferation via targeting Jarid2.

Authors: Liang, D  Li, J  Wu, Y  Zhen, L  Li, C  Qi, M  Wang, L  Deng, F  Huang, J  Lv, F  Liu, Y  Ma, X  Yu, Z  Zhang, Y  Chen, YH 
Citation: Liang D, etal., Int J Cardiol. 2015 Dec 15;201:38-48. doi: 10.1016/j.ijcard.2015.06.163. Epub 2015 Jul 2.
Pubmed: (View Article at PubMed) PMID:26298346
DOI: Full-text: DOI:10.1016/j.ijcard.2015.06.163

OBJECTIVES: In mammals, the heart grows by hypertrophy but not proliferation of cardiomyocytes after birth. The paucity of cardiomyocyte proliferation limits cardiac regeneration in a variety of heart diseases. To explore the efficient strategies that drive cardiomyocyte proliferation, we employed in vitro and in vivo models to investigate the function of miRNA-204, which was demonstrated to regulate the proliferation and differentiation of human cardiac progenitor cells in our previous study. METHODS AND RESULTS: miRNA-204 overexpression markedly promoted cardiomyocyte proliferation in both neonatal and adult rat cardiomyocytes in vitro. Transgenic mice with the cardiac-specific overexpression of miRNA-204 exhibited excessive cardiomyocyte proliferation throughout the embryonic and adult stages, leading to a pronounced increase in ventricular mass. Accordingly, the cell cycle regulators, including Cyclin A, Cyclin B, Cyclin D2, Cyclin E, CDC2 and PCNA, were upregulated in miRNA-204 transgenic embryonic hearts. Furthermore, we demonstrated that miRNA-204 directly targeted Jarid2. Knockdown of Jarid2 mimicked the pro-proliferative effect of miRNA-204 overexpression on cultured rat cardiomyocytes, whereas enhanced expression of Jarid2 conferred the myocytes with substantial resistance to proliferation by miRNA-204 overexpression. CONCLUSION: Our findings identify a conserved role for miRNA-204 in regulating cardiomyocyte proliferation by targeting the Jarid2 signaling pathway.


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CRRD Object Information
CRRD ID: 11522645
Created: 2016-08-03
Species: All species
Last Modified: 2016-08-03
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.