Abstract
Oxidative myofibers are resistant to catabolic wasting caused by many chronic diseases, such as congestive heart failure and sepsis. We have recently identified a nitric oxide‐dependent antioxidant defense mechanism in this oxidative phenotype‐associated protection. Here, we show that systemic administration of NO donor GSNO (4 mg/kg/day, i.p.) significantly suppressed glucocorticoid‐induced (dexamethasone, 25 mg/kg/day, i.p.) loss of muscle mass and increases in E3 ligases MAFbx/atrogin‐1 mRNA expression in glyocolytic muscles. GSNO also prevented dexamethasone‐induced reduction of superoxide dismutase 3 (SOD3) protein expression. Importantly, somatic gene transfer of SOD3 in glycolytic tibialis anterior muscle significantly attenuated dexamethasone‐induced muscle atrophy. These findings suggest the functional importance of SOD3 in NO‐mediated protection against catabolic wasting in skeletal muscle.
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