IFRD2, a target of miR-2400, regulates myogenic differentiation of bovine skeletal muscle satellite cells via decreased phosphorylation of ERK1/2 proteins.

IF 1.8 3区 生物学 Q4 CELL BIOLOGY
Zhian Gong, Xiaoyu Zhang, Jingxuan Cui, Wen Chen, Xin Huang, Qingzhu Yang, Tie Li, Weiwei Zhang
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Abstract

The proliferation and differentiation of skeletal muscle satellite cells is a complex physiological process involving various transcription factors and small RNA molecules. This study aimed to understand the regulatory mechanisms underlying these processes, focusing on interferon-related development factor 2 (IFRD2) as a target gene of miRNA-2400 in bovine skeletal MuSCs (MuSCs). IFRD2 was identified as a target gene of miRNA-2400 involved in regulating the proliferation and differentiation of bovine skeletal MuSCs. Our results indicate that miR-2400 can target binding the 3'UTR of IFRD2 and inhibit its translation. mRNA and protein expression levels of IFRD2 increased significantly with increasing days of differentiation. Moreover, overexpression of the IFRD2 gene inhibited proliferation and promoted differentiation of bovine MuSCs. Conversely, the knockdown of the gene had the opposite effect. Overexpression of IFRD2 resulted in the inhibition of ERK1/2 phosphorylation levels in bovine MuSCs, which in turn promoted differentiation. In summary, IFRD2, as a target gene of miR-2400, crucially affects bovine skeletal muscle proliferation and differentiation by precisely regulating ERK1/2 phosphorylation.

Abstract Image

miR-2400 的靶标 IFRD2 通过减少 ERK1/2 蛋白的磷酸化调节牛骨骼肌卫星细胞的成肌分化。
骨骼肌卫星细胞的增殖和分化是一个复杂的生理过程,涉及各种转录因子和小 RNA 分子。本研究旨在了解这些过程的调控机制,重点研究牛骨骼肌卫星细胞(MuSCs)中作为 miRNA-2400 靶基因的干扰素相关发育因子 2(IFRD2)。研究发现,IFRD2 是 miRNA-2400 参与调控牛骨骼 MuSCs 增殖和分化的靶基因。我们的研究结果表明,miR-2400 能靶向结合 IFRD2 的 3'UTR 并抑制其翻译。随着分化天数的增加,IFRD2 的 mRNA 和蛋白表达水平显著增加。此外,过表达 IFRD2 基因可抑制牛 MuSCs 的增殖并促进其分化。相反,敲除该基因则会产生相反的效果。过表达 IFRD2 可抑制牛 MuSCs 的 ERK1/2 磷酸化水平,进而促进分化。综上所述,IFRD2作为miR-2400的靶基因,通过精确调控ERK1/2磷酸化,对牛骨骼肌的增殖和分化产生了至关重要的影响。
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来源期刊
CiteScore
6.20
自引率
0.00%
发文量
21
审稿时长
>12 weeks
期刊介绍: The Journal of Muscle Research and Cell Motility has as its main aim the publication of original research which bears on either the excitation and contraction of muscle, the analysis of any one of the processes involved therein, the processes underlying contractility and motility of animal and plant cells, the toxicology and pharmacology related to contractility, or the formation, dynamics and turnover of contractile structures in muscle and non-muscle cells. Studies describing the impact of pathogenic mutations in genes encoding components of contractile structures in humans or animals are welcome, provided they offer mechanistic insight into the disease process or the underlying gene function. The policy of the Journal is to encourage any form of novel practical study whatever its specialist interest, as long as it falls within this broad field. Theoretical essays are welcome provided that they are concise and suggest practical ways in which they may be tested. Manuscripts reporting new mutations in known disease genes without validation and mechanistic insight will not be considered. It is the policy of the journal that cells lines, hybridomas and DNA clones should be made available by the developers to any qualified investigator. Submission of a manuscript for publication constitutes an agreement of the authors to abide by this principle.
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