Key result
GSK3β inhibition promoted skeletal muscle satellite cell differentiation and regulated MyHC2a gene expression through NFATc2 in goat-differentiated SMSCs.
Why the study?
GSK3β is important in skeletal muscle growth and repair, but the mechanism by which it regulates MyHC2a expression remains unclear.
GSK3β inhibition promotes differentiation of goat skeletal muscle satellite cells and regulates MyHC2a expression via the NFATc2 element.
May inform muscle regeneration strategies; leaves open translation to human cardiac or skeletal applications.
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.
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Wang et al. (2019) studied this question. GSK3β inhibition (SB216713) was evaluated on MyHC2a gene expression and promoter activity. GSK3β inhibition promoted skeletal muscle satellite cell differentiation and regulated MyHC2a gene expression through NFATc2 in goat-differentiated SMSCs.
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