Inhibitory effect of SMAD2 on myogenesis in heat-stressed Hu sheep myoblasts

Heat stress can cause muscle damage and affect myogenesis. Myogenesis is a complicated process modulated by numerous genes. While SMAD2 has been implicated in various biological processes, its specific role in the myogenesis of heat-stressed Hu sheep myoblasts remains unclear. To explore the function of SMAD2 in myogenesis, si-SMAD2-446 and pcDNA3.1-SMAD2 were transfected into heat-stressed Hu sheep myoblasts. The results indicated that heat stress increased the SMAD2 expression in Hu sheep myoblasts. Furthermore, SMAD2 was found to suppress proliferation in heat-stressed Hu sheep myoblasts by downregulating the expression of proliferation-related genes, including proliferating cell nuclear antigen (PCNA), cyclin D1 (CCND1) and cyclin-dependent kinase 2 (CDK2). Additionally, SMAD2 inhibited differentiation by downregulating the expression of myogenic differentiation factor (MYOD) and myogenin (MYOG). Moreover, SMAD2 promoted apoptosis by activating BCL-associated X protein (BAX), B-cell CLL/lymphoma 2 (BCL-2), Caspase3 and Caspase9 in heat-stressed Hu sheep myoblasts. In conclusion, these findings suggest that SMAD2 functions as an inhibitory factor in the myogenesis of heat-stressed Hu sheep myoblasts.