bta-miR-23a Regulates the Myogenic Differentiation of Fetal Bovine Skeletal Muscle-Derived Progenitor Cells by Targeting MDFIC Gene
Autor: | Lingyang Xu, Lupei Zhang, Qian Li, Xin Hu, Qiyuan Yang, Yishen Xing, Min Du, Ling Ren, Luc Willems, Junya Li, Yahui Wang |
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Jazyk: | angličtina |
Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
Untranslated region lcsh:QH426-470 MDFIC Muscle Development Article 03 medical and health sciences 0302 clinical medicine Downregulation and upregulation Genetics medicine Animals MEF2C Progenitor cell bta-miR-23a Muscle Skeletal Transcription factor Genetics (clinical) Gene knockdown Chemistry Stem Cells Gene Expression Regulation Developmental Skeletal muscle Cell Differentiation Cell biology MicroRNAs lcsh:Genetics 030104 developmental biology medicine.anatomical_structure Myogenic Regulatory Factors fetal muscle development 030220 oncology & carcinogenesis Cattle MyoD family inhibitor |
Zdroj: | Genes, Vol 11, Iss 1232, p 1232 (2020) Genes Volume 11 Issue 10 |
ISSN: | 2073-4425 |
Popis: | 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 &minus 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&rsquo 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. |
Databáze: | OpenAIRE |
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