Bta-miR-24-3p Controls the Myogenic Differentiation and Proliferation of Fetal, Bovine, Skeletal Muscle-Derived Progenitor Cells by Targeting ACVR1B
Authors
Xing, YishenHu, Xin
Ren, Ling
Wang, Yahui
Li, Qian
Fu, Xing
Yang, Qiyuan
Xu, Lingyang
Willems, Luc
Li, Junya
Zhang, Lupei
Xing, Yishen
Ren, Ling
Wang, Yahui
Li, Qian
Fu, Xing
Yang, Qiyuan
Xu, Lingyang
Willems, Luc
Li, Junya
Zhang, Lupei
UMass Chan Affiliations
Department of Molecular, Cell and Cancer BiologyDocument Type
Journal ArticlePublication Date
2019-10-24Keywords
bta-miR-24-3pbovine
fetal skeletal muscle
proliferation
differentiation
ACVR1B
Amino Acids, Peptides, and Proteins
Cell Biology
Cells
Developmental Biology
Nucleic Acids, Nucleotides, and Nucleosides
Metadata
Show full item recordAbstract
MicroRNAs modulate a variety of cellular events, including skeletal muscle development, but the molecular basis of their functions in fetal bovine skeletal muscle development is poorly understood. In this study, we report that bta-miR-24-3p promotes the myogenic differentiation of fetal bovine PDGFRalpha(-) progenitor cells. The expression of bta-miR-24-3p increased during myogenic differentiation. Overexpression of bta-miR-24-3p significantly promoted myogenic differentiation, but inhibited proliferation. A dual-luciferase assay identified ACVR1B as a direct target of bta-miR-24-3p. Similarly, knocking down ACVR1B by RNA interference also significantly inhibited proliferation and promoted the differentiation of bovine PDGFRalpha(-) progenitor cells. Thus, our study provides a mechanism in which bta-miR-24-3p regulates myogenesis by inhibiting ACVR1B expression.Source
Animals (Basel). 2019 Oct 24;9(11). pii: ani9110859. doi: 10.3390/ani9110859. Link to article on publisher's site
DOI
10.3390/ani9110859Permanent Link to this Item
http://hdl.handle.net/20.500.14038/41221PubMed ID
31652908Related Resources
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© 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).Distribution License
http://creativecommons.org/licenses/by/4.0/ae974a485f413a2113503eed53cd6c53
10.3390/ani9110859
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Except where otherwise noted, this item's license is described as © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).