bta-miR-23a Regulates the Myogenic Differentiation of Fetal Bovine Skeletal Muscle-Derived Progenitor Cells by Targeting MDFIC Gene

文献类型： 外文期刊

第一作者： Hu, Xin

作者： Hu, Xin;Xing, Yishen;Ren, Ling;Wang, Yahui;Li, Qian;Xu, Lingyang;Li, Junya;Zhang, Lupei;Hu, Xin;Willems, Luc;Yang, Qiyuan;Du, Min;Du, Min

作者机构：

关键词： bta-miR-23a; fetal muscle development; MDFIC

期刊名称：GENES （ 影响因子：4.096； 五年影响因子：4.339 ）

ISSN：

年卷期： 2020 年 11 卷 10 期

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收录情况： SCI

摘要： miR-23a, a member of the miR-23a/24-2/27a cluster, has been demonstrated to play pivotal roles in many cellular activities. However, the mechanisms of how bta-miR-23a controls the myogenic differentiation (MD) of PDGFR alpha(-) bovine progenitor cells (bPCs) remain poorly understood. In the present work, bta-miR-23a expression was increased during the MD of (PDGFR alpha-) bPCs. Moreover, bta-miR-23a overexpression significantly promoted the MD of (PDGFR alpha-) bPCs. Luciferase reporter assays showed that the 3'-UTR region of MDFIC (MyoD family inhibitor domain containing) could be a promising target of bta-miR-23a, which resulted in its post-transcriptional down-regulation. Additionally, the knockdown of MDFIC by siRNA facilitated the MD of (PDGFR alpha-) bPCs, while the overexpression of MDFIC inhibited the activating effect of bta-miR-23a during MD. Of note, MDFIC might function through the interaction between MyoG transcription factor and MEF2C promoter. This study reveals that bta-miR-23a can promote the MD of (PDGFR alpha-) bPCs through post-transcriptional downregulation of MDFIC.

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