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

International Journal of Molecular Sciences

Ya-Han Wu¹  Hong Zhao²  Li-Ping Zhou¹  Chun-Xia Zhao¹  Yu-Fei Wu¹  Li-Xiao Zhen¹  Jun Li¹  Dong-Xia Ge¹  Liang Xu¹  Li Lin¹  Yi Liu¹  Dan-Dan Liang¹  Yi-Han Chen¹ 

[1] Key Laboratory of Arrhythmias of the Ministry of Education of China, East Hospital, Tongji University School of Medicine, Shanghai 200120, China; E-Mails:;Department of Pediatrics, Tongji Hospital, Tongji University, Shanghai 200120, China; E-Mail:

关键词: hCMPCs;    miR-134;    proliferation;    Meis2;   

DOI  :  10.3390/ijms161025199

来源: mdpi

【 摘 要 】

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.

【 授权许可】

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© 2015 by the authors; licensee MDPI, Basel, Switzerland.