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Int. J. Mol. Sci. 2015, 16(10), 25199-25213; doi:10.3390/ijms161025199

miR-134 Modulates the Proliferation of Human Cardiomyocyte Progenitor Cells by Targeting Meis2

1,2,3,4,†
,
5,†
,
1,4,†
,
1,3,4,†
,
1,4
,
1,4
,
1,2,3
,
1,2,3
,
1,2,3
,
1,2,3
,
1,2,3
,
1,2,3
and
1,2,3,4,6,*
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 Pediatrics, Tongji Hospital, Tongji University, Shanghai 200120, China
6
Department of Pathology and Pathophysiology, Tongji University School of Medicine, Shanghai 200092, China
These authors contributed equally to this work.
*
Author to whom correspondence should be addressed.
Academic Editor: H. W. M. Niessen
Received: 18 June 2015 / Revised: 16 September 2015 / Accepted: 25 September 2015 / Published: 23 October 2015
(This article belongs to the Special Issue Improvement of Cardiac Function in Heart Failure)
View Full-Text   |   Download PDF [2124 KB, uploaded 23 October 2015]   |  

Abstract

Cardiomyocyte progenitor cells play essential roles in early heart development, which requires highly controlled cellular organization. microRNAs (miRs) are involved in various cell behaviors by post-transcriptional regulation of target genes. However, the roles of miRNAs in human cardiomyocyte progenitor cells (hCMPCs) remain to be elucidated. Our previous study showed that miR-134 was significantly downregulated in heart tissue suffering from congenital heart disease, underlying the potential role of miR-134 in cardiogenesis. In the present work, we showed that the upregulation of miR-134 reduced the proliferation of hCMPCs, as determined by EdU assay and Ki-67 immunostaining, while the inhibition of miR-134 exhibited an opposite effect. Both up- and downregulation of miR-134 expression altered the transcriptional level of cell-cycle genes. We identified Meis2 as the target of miR-134 in the regulation of hCMPC proliferation through bioinformatic prediction, luciferase reporter assay and western blot. The over-expression of Meis2 mitigated the effect of miR-134 on hCMPC proliferation. Moreover, miR-134 did not change the degree of hCMPC differentiation into cardiomyocytes in our model, suggesting that miR-134 is not required in this process. These findings reveal an essential role for miR-134 in cardiomyocyte progenitor cell biology and provide new insights into the physiology and pathology of cardiogenesis. View Full-Text
Keywords: hCMPCs; miR-134; proliferation; Meis2 hCMPCs; miR-134; proliferation; Meis2
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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Wu, Y.-H.; Zhao, H.; Zhou, L.-P.; Zhao, C.-X.; Wu, Y.-F.; Zhen, L.-X.; Li, J.; Ge, D.-X.; Xu, L.; Lin, L.; Liu, Y.; Liang, D.-D.; Chen, Y.-H. miR-134 Modulates the Proliferation of Human Cardiomyocyte Progenitor Cells by Targeting Meis2. Int. J. Mol. Sci. 2015, 16, 25199-25213.

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