Glycogen synthase kinase 3β (GSK3β) regulates the expression of MyHC2a in goat skeletal muscle satellite cells (SMSCs).
Linjie WangYuehua ZhuXin LiuZhe ChaoYan WangTao ZhongJiazhong GuoSiyuan ZhanLi LiHongping ZhangPublished in: Animal science journal = Nihon chikusan Gakkaiho (2019)
Glycogen synthase kinase beta (GSK3β) plays an important role in skeletal muscle growth, regeneration, and repair. However, the mechanism of GSK3β regulating MyHC2a expression is currently not clear. In this study, GSK3β 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, GSK3β inhibition had no effect on the luciferase activity of MyHC2a promoter after mutating the NFATc2-binding site. These results demonstrated that GSK3β inhibition promoted SMSCs differentiation and regulated the MyHC2a gene expression through NFATc2 in goat-differentiated SMSCs.
Keyphrases
- gene expression
- skeletal muscle
- dna methylation
- pi k akt
- signaling pathway
- transcription factor
- induced apoptosis
- cell cycle arrest
- poor prognosis
- genome wide
- insulin resistance
- stem cells
- binding protein
- oxidative stress
- tyrosine kinase
- type diabetes
- genome wide identification
- endoplasmic reticulum stress
- cell death
- cell proliferation