肌发生
肌肉萎缩
下调和上调
萎缩
基因敲除
骨骼肌
C2C12型
基因表达
生物
免疫印迹
心肌细胞
小RNA
基因
内分泌学
内科学
分子生物学
细胞生物学
医学
遗传学
作者
Xin Yang,Zhenhui Li,Zhijun Wang,Jiaao Yu,Manting Ma,Qinghua Nie
出处
期刊:Biomolecules
[Multidisciplinary Digital Publishing Institute]
日期:2022-01-23
卷期号:12 (2): 191-191
被引量:8
摘要
As it is well known, muscle atrophy is a process in which protein degradation increases and protein synthesis decreases. This process is regulated by a variety of links. Among them, microRNAs play an essential role in this process, which has attracted widespread attention. In this paper, we find that miR-27b-3p and Cbl-b genes are significantly differentially expressed in the induced atrophy model. The dual-luciferase experiment and Western blot analysis confirmed that miR-27b-3p could regulate the expression of Cbl-b. In C2C12-differentiated myotubes, the overexpression of the Cbl-b gene showed that Cbl-b could upregulate the expression of MuRF-1 and Atrogin-1, which are related marker genes of muscle atrophy, at both the mRNA and protein levels, indicating that the Cbl-b gene can specifically affect muscle atrophy. The knockdown of the Cbl-b gene after C2C12-differentiated myotubes induced atrophy treatment can downregulate the expression of muscle-atrophy-related genes, indicating that manual intervention to downregulate the expression of Cbl-b has a certain alleviating effect on muscle atrophy. These data suggest that miR-27b-3p can regulate the expression of the Cbl-b gene and then exert a particular influence on muscle atrophy through the Cbl-b gene.
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