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miR-205 通过靶向 Myomaker 基因调节猪成肌细胞的融合。

miR-205 Regulates the Fusion of Porcine Myoblast by Targeting the Myomaker Gene.

机构信息

Chongqing Academy of Animal Sciences, Chongqing 402460, China.

Key Laboratory of Pig Industry Sciences, Ministry of Agriculture, Chongqing 402460, China.

出版信息

Cells. 2023 Apr 7;12(8):1107. doi: 10.3390/cells12081107.

DOI:10.3390/cells12081107
PMID:37190016
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10136817/
Abstract

Skeletal muscle formation is an extremely important step in animal growth and development. Recent studies have found that TMEM8c (also known as Myomaker, MYMK), a muscle-specific transmembrane protein, can promote myoblast fusion and plays a key role in the normal development of skeletal muscle. However, the effect of Myomaker on porcine () myoblast fusion and the underlying regulatory mechanisms remain largely unknown. Therefore, in this study, we focused on the role and corresponding regulatory mechanism of the gene during skeletal muscle development, cell differentiation, and muscle injury repair in pigs. We obtained the entire 3' UTR sequence of porcine using the 3' RACE approach and found that miR-205 inhibited porcine myoblast fusion by targeting the 3' UTR of . In addition, based on a constructed porcine acute muscle injury model, we discovered that both the mRNA and protein expression of were activated in the injured muscle, while miR-205 expression was significantly inhibited during skeletal muscle regeneration. The negative regulatory relationship between miR-205 and Myomaker was further confirmed in vivo. Taken together, the present study reveals that Myomaker plays a role during porcine myoblast fusion and skeletal muscle regeneration and demonstrates that miR-205 inhibits myoblast fusion through targeted regulation of the expression of Myomaker.

摘要

骨骼肌的形成是动物生长和发育过程中的一个极其重要的步骤。最近的研究发现,TMEM8c(也称为 Myomaker、MYMK),一种肌肉特异性跨膜蛋白,可促进成肌细胞融合,在骨骼肌的正常发育中发挥关键作用。然而,Myomaker 对猪()成肌细胞融合的影响及其潜在的调节机制在很大程度上仍然未知。因此,在这项研究中,我们专注于 基因在猪骨骼肌发育、细胞分化和肌肉损伤修复过程中的作用及其相应的调节机制。我们使用 3' RACE 方法获得了猪 的完整 3'UTR 序列,并发现 miR-205 通过靶向 的 3'UTR 抑制猪成肌细胞融合。此外,基于构建的猪急性肌肉损伤模型,我们发现 基因在损伤肌肉中的 mRNA 和蛋白表达均被激活,而 miR-205 的表达在骨骼肌再生过程中显著受到抑制。miR-205 与 Myomaker 之间的负调控关系在体内得到了进一步证实。总之,本研究揭示了 Myomaker 在猪成肌细胞融合和骨骼肌再生过程中发挥作用,并表明 miR-205 通过靶向调节 Myomaker 的表达来抑制成肌细胞融合。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e15/10136817/7e5f97f2ebdd/cells-12-01107-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e15/10136817/0bb2b87d4a34/cells-12-01107-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e15/10136817/035e86eded4b/cells-12-01107-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e15/10136817/2c9cb730fff9/cells-12-01107-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e15/10136817/2b653edb4b63/cells-12-01107-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e15/10136817/a69e66bd9c88/cells-12-01107-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e15/10136817/815408645b88/cells-12-01107-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e15/10136817/7e5f97f2ebdd/cells-12-01107-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e15/10136817/0bb2b87d4a34/cells-12-01107-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e15/10136817/035e86eded4b/cells-12-01107-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e15/10136817/2c9cb730fff9/cells-12-01107-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e15/10136817/2b653edb4b63/cells-12-01107-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e15/10136817/a69e66bd9c88/cells-12-01107-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e15/10136817/815408645b88/cells-12-01107-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e15/10136817/7e5f97f2ebdd/cells-12-01107-g007.jpg

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