Arginine Promotes Slow Myosin Heavy Chain Expression via Akirin2 and the AMP-Activated Protein Kinase Signaling Pathway in Porcine Skeletal Muscle Satellite Cells

This study aimed to investigate the effect of arginine on the expression of slow myosin heavy chain (MyHC) I and its underlying mechanism in porcine skeletal muscle satellite cells. Our results showed that arginine upregulated the mRNA (1.54 ± 0.08; p < 0.01) and protein (2.01 ± 0.01; p < 0.001) levels of MyHC I. We also showed that arginine upregulated the expression of Akirin2 (1.35 ± 0.1; p < 0.05) and increased the NO content (1.56 ± 0.04; p < 0.001). Akirin2 siRNA abolished arginine-induced upregulation of MyHC I and the increase of the NO content. In addition, arginine significantly increased the phospho-AMP-activated protein kinase (AMPK)/AMPK level (1.33 ± 0.06; p < 0.05), the AMPK content (79.55 ± 0.13; p < 0.001), and the AMPKα2 mRNA level (2.03 ± 0.20; p < 0.01). AMPKα2 silencing or AMPK inhibitor Compound C abolished arginine-induced upregulation of MyHC I. Our results provide, for the first time, evidence for the involvement of Akirin2 and the AMPK signaling pathway in arginine-induced MyHC I expression in porcine skeletal muscle satellite cells.