miR-2400 promotes proliferation of bovine skeletal muscle-derived satellite cells by regulating MAGED1 genes expression.

IF 1.8 3区 生物学 Q4 CELL BIOLOGY
Li Yang, Hai-Jing Luo, Zhi-An Gong, Wen-Tian Zhang, Jing-Xuan Cui, Xue-Peng Fu, Wei-Wei Zhang
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引用次数: 0

Abstract

microRNAs play a crucial role in the intricate process of muscle satellite cells proliferation and differentiation. Previous studies have demonstrated that miR-2400 can regulate bovine skeletal muscle satellite cell (MuSCs) proliferation, yet the underlying mechanism remains incompletely elucidated. In this study, we employed bioinformatics prediction and dual luciferase reporter assays to establish that miR-2400 directly targets the 3' untranslated regions (UTRs) of melanoma antigen family D1 (MAGED1) mRNA, thereby suppressing its expression. To ascertain whether miR-2400 affects the proliferation of MuSCs through MAGED1, we constructed the MAGED1 interference vector using RNA interference technology (RNAi) and assessed changes in MuSCs proliferation subsequent to MAGED1 interference. The experimental data indicate that the cell viability and the rate of EdU-positive cells of MuSCs were increased after interference with MAGED1. The proportion of S-phase cells and the expression level of cell cycle-associated proteins CCND2 and CCNB1 increased. These findings align with miR-2400's role in promoting cell proliferation and suggest that miR-2400 exerts its effects by directly targeting MAGED1.

miR-2400通过调节MAGED1基因表达促进牛骨骼肌来源卫星细胞的增殖。
microrna在肌卫星细胞增殖和分化的复杂过程中起着至关重要的作用。先前的研究表明,miR-2400可以调节牛骨骼肌卫星细胞(MuSCs)的增殖,但其潜在机制尚未完全阐明。在本研究中,我们采用生物信息学预测和双荧光素酶报告基因检测来确定miR-2400直接靶向黑色素瘤抗原家族D1 (MAGED1) mRNA的3'非翻译区(UTRs),从而抑制其表达。为了确定miR-2400是否通过MAGED1影响musc的增殖,我们使用RNA干扰技术(RNAi)构建了MAGED1干扰载体,并评估了MAGED1干扰后musc增殖的变化。实验数据表明,干扰MAGED1后,细胞活力和edu阳性细胞率均有所提高。s期细胞比例及细胞周期相关蛋白CCND2、CCNB1表达水平升高。这些发现与miR-2400在促进细胞增殖中的作用一致,并表明miR-2400通过直接靶向MAGED1发挥其作用。
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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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