Abstract
Myoblast differentiation and fusion are vital for muscle development and repair in mammals. We previously showed that necrostatin-1(Nec-1) protects C2C12 myotubes from cobalt chloride (CoCl2)-induced pseudo-hypoxia. However, the function of Nec-1 in mouse C2C12 myoblast differentiation and fusion was still unknown. In this study, we found that CoCl2 substantially impaired C2C12 myoblast differentiation and fusion, and reduced the expression of Myh1, Myh2, Myh4, Myh7, myomaker, and myomerger. Nec-1 treatment rescued C2C12 myoblast differentiation and fusion and promoted the expression of myomaker and myomerger. Mechanistically, Nec-1 promoted C2C12 myoblast differentiation and fusion by inhibiting mTOR-mediated autophagy. Rapamycin abolished the increases in expression of muscle fusion-related genes, indicating that the upregulation of differentiation and fusion is mTOR-dependent. These results suggest that Nec-1 inhibited autophagy in an mTOR-dependent mechanism that is crucial for mTOR-induced C2C12 myoblast differentiation and fusion.
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