| Summary: | 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<sup>−</sup> bovine progenitor cells (bPCs) remain poorly understood. In the present work, bta-miR-23a expression was increased during the MD of <sup>PDGFRα−</sup> bPCs. Moreover, bta-miR-23a overexpression significantly promoted the MD of <sup>PDGFRα−</sup> bPCs. Luciferase reporter assays showed that the 3’-UTR region of <i>MDFIC</i> (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 <i>MDFIC</i> by siRNA facilitated the MD of <sup>PDGFRα−</sup> bPCs, while the overexpression of <i>MDFIC</i> inhibited the activating effect of bta-miR-23a during MD. Of note, <i>MDFIC</i> might function through the interaction between <i>MyoG</i> transcription factor and <i>MEF2C</i> promoter. This study reveals that bta-miR-23a can promote the MD of <sup>PDGFRα−</sup> bPCs through post-transcriptional downregulation of <i>MDFIC</i>.
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