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miRNA-1调控对于雄性小鼠机械负荷诱导的肌肉肥大是必要的。

miRNA-1 regulation is necessary for mechanical overload-induced muscle hypertrophy in male mice.

作者信息

Fei Shengyi, Rule Blake D, Godwin Joshua S, Mobley C Brooks, Roberts Michael D, von Walden Ferdinand, Vechetti Ivan J

机构信息

Department of Nutrition and Health Sciences, University of Nebraska-Lincoln, Lincoln, Nebraska, USA.

School of Kinesiology, Auburn University, Auburn, Alabama, USA.

出版信息

Physiol Rep. 2025 Jan;13(1):e70166. doi: 10.14814/phy2.70166.

DOI:10.14814/phy2.70166
PMID:39761956
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11705529/
Abstract

MicroRNAs (miRNAs) are small, noncoding RNAs that play a critical role in regulating gene expression post-transcriptionally. They are involved in various developmental and physiological processes, and their dysregulation is linked to various diseases. Skeletal muscle-specific miRNAs, including miR-1, play a crucial role in the development and maintenance of skeletal muscle. It has been demonstrated that the expression of miR-1 decreases by approximately 50% in response to hypertrophic stimuli, suggesting its potential involvement in muscle hypertrophy. In our study, we hypothesize that reduction of miR-1 levels is necessary for skeletal muscle growth due to its interaction to essential pro-growth genes. Promoting a smaller reduction of miR-1 levels, we observed a blunted hypertrophic response in mice undergoing a murine model of muscle hypertrophy. In addition, our results suggest that miR-1 inhibits the expression of Itm2a, a membrane-related protein, as potential miR-1-related candidate for skeletal muscle hypertrophy. While the exact mechanism in muscle hypertrophy has not been identified, our results suggest that miR-1-regulated membrane proteins are important for skeletal muscle hypertrophy.

摘要

微小RNA(miRNA)是一类小的非编码RNA,在转录后调控基因表达中发挥关键作用。它们参与各种发育和生理过程,其失调与多种疾病相关。包括miR-1在内的骨骼肌特异性miRNA在骨骼肌的发育和维持中起关键作用。已经证明,在肥大刺激下,miR-1的表达下降约50%,这表明其可能参与肌肉肥大。在我们的研究中,我们假设由于miR-1与重要的促生长基因相互作用,其水平降低对于骨骼肌生长是必要的。在促进miR-1水平较小程度降低的情况下,我们在经历肌肉肥大小鼠模型的小鼠中观察到肥大反应减弱。此外,我们的结果表明,miR-1抑制Itm2a(一种膜相关蛋白)的表达,Itm2a是骨骼肌肥大潜在的miR-1相关候选蛋白。虽然肌肉肥大的确切机制尚未确定,但我们的结果表明,miR-1调控的膜蛋白对骨骼肌肥大很重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a75/11705529/7742f7694bd5/PHY2-13-e70166-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a75/11705529/d5594372033e/PHY2-13-e70166-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a75/11705529/d76c9d27e5b4/PHY2-13-e70166-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a75/11705529/e84e4e516886/PHY2-13-e70166-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a75/11705529/e39ce4f785e0/PHY2-13-e70166-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a75/11705529/7742f7694bd5/PHY2-13-e70166-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a75/11705529/d5594372033e/PHY2-13-e70166-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a75/11705529/d76c9d27e5b4/PHY2-13-e70166-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a75/11705529/e84e4e516886/PHY2-13-e70166-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a75/11705529/e39ce4f785e0/PHY2-13-e70166-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a75/11705529/7742f7694bd5/PHY2-13-e70166-g006.jpg

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