Glycogen synthase kinase 3 beta (GSK3 beta) regulates the expression of MyHC2a in goat skeletal muscle satellite cells (SMSCs)
文献类型： 外文期刊
作者： Wang, Linjie 1 ; Zhu, Yuehua 1 ; Liu, Xin 1 ; Chao, Zhe 2 ; Wang, Yan 1 ; Zhong, Tao 1 ; Guo, Jiazhong 1 ; Zhan, Siyuan 1 ;
作者机构： 1.Sichuan Agr Univ, Coll Anim Sci & Technol, Farm Anim Genet Resources Explorat & Innovat Key, Chengdu, Sichuan, Peoples R China
2.Hainan Acad Agr Sci, Inst Anim Sci & Vet Med, Haikou, Hainan, Peoples R China
关键词： goat; GSK3 beta; MyHC2a; promoter; satellite cells
期刊名称：ANIMAL SCIENCE JOURNAL （ 影响因子：1.749； 五年影响因子：1.909 ）
ISSN： 1344-3941
年卷期： 2019 年 90 卷 8 期
页码：
收录情况： SCI
摘要： Glycogen synthase kinase beta (GSK3 beta) plays an important role in skeletal muscle growth, regeneration, and repair. However, the mechanism of GSK3 beta regulating MyHC2a expression is currently not clear. In this study, GSK3 beta inhibition promoted skeletal muscle satellite cells (SMSCs) differentiation and increased expression of MyoD, MyoG, MyHC1, and MyHC2a genes. Then we cloned approximately 1.1 kb of goat MyHC2a gene promoter. The deletion fragment (-514/+55) of MyHC2a promoter exhibited the highest level of promoter activity, and a NFATc2 element in this region was responsible for MyHC2a promoter activity. Treatment of SB216713 significantly decreased the transcriptional activity of the fragment (-514/+55). Furthermore, GSK3 beta inhibition had no effect on the luciferase activity of MyHC2a promoter after mutating the NFATc2-binding site. These results demonstrated that GSK3 beta inhibition promoted SMSCs differentiation and regulated the MyHC2a gene expression through NFATc2 in goat-differentiated SMSCs.
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