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 PDGFRα− bovine progenitor cells (bPCs) remain poorly understood. In the present work, bta-miR-23a expression was increased during the MD of PDGFRα− bPCs. Moreover, bta-miR-23a overexpression significantly promoted the MD of PDGFRα− 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 PDGFRα− 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 PDGFRα− bPCs through post-transcriptional downregulation of MDFIC.

中文翻译：

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bta-miR-23a 通过靶向 MDFIC 基因调控胎牛骨骼肌源性祖细胞的生肌分化

miR-23a 是 miR-23a/24-2/27a 簇的成员，已被证明在许多细胞活动中发挥关键作用。然而，bta-miR-23a 如何控制 PDGFRα-牛祖细胞 (bPC) 的肌源性分化 (MD) 的机制仍然知之甚少。在目前的工作中，bta-miR-23a 表达在 PDGFRα-bPC 的 MD 期间增加。此外，bta-miR-23a 过表达显着促进了 PDGFRα-bPC 的 MD。荧光素酶报告基因检测表明，MDFIC 的 3'-UTR 区域（含有 MyoD 家族抑制剂域）可能是 bta-miR-23a 的一个有希望的靶标，这导致其转录后下调。此外，siRNA对MDFIC的敲低促进了PDGFRα-bPC的MD，而MDFIC的过表达抑制了MD期间bta-miR-23a的激活作用。值得注意的是，MDFIC 可能通过 MyoG 转录因子和 MEF2C 启动子之间的相互作用起作用。该研究表明，bta-miR-23a 可以通过 MDFIC 的转录后下调来促进 PDGFRα-bPC 的 MD。