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,
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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.
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