scholarly journals bta-miR-23a involves in adipogenesis of progenitor cells derived from fetal bovine skeletal muscle

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Long Guan ◽  
Xin Hu ◽  
Li Liu ◽  
Yishen Xing ◽  
Zhengkui Zhou ◽  
...  
Animals ◽  
2019 ◽  
Vol 9 (11) ◽  
pp. 859 ◽  
Author(s):  
Xin Hu ◽  
Yishen Xing ◽  
Ling Ren ◽  
Yahui Wang ◽  
Qian Li ◽  
...  

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 PDGFRα- 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 PDGFRα- progenitor cells. Thus, our study provides a mechanism in which bta-miR-24-3p regulates myogenesis by inhibiting ACVR1B expression.


Genes ◽  
2020 ◽  
Vol 11 (10) ◽  
pp. 1232
Author(s):  
Xin Hu ◽  
Yishen Xing ◽  
Ling Ren ◽  
Yahui Wang ◽  
Qian Li ◽  
...  

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.


2005 ◽  
Vol 18 (6) ◽  
pp. 884-891
Author(s):  
S. Yamamoto ◽  
B. Gerelt ◽  
T. Nishiumi ◽  
A. Suzuki

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