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

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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Detalles Bibliográficos
Autores principales: Hu, Xin, Xing, Yishen, Ren, Ling, Wang, Yahui, Li, Qian, Yang, Qiyuan, Du, Min, Xu, Lingyang, Willems, Luc, Li, Junya, Zhang, Lupei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7588927/
https://www.ncbi.nlm.nih.gov/pubmed/33092227
http://dx.doi.org/10.3390/genes11101232
Descripción
Sumario: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.