CSE-driven myofiber wasting suppresses myogenic factor production without impacting on atrophy related genes
In humans, smoking has been demonstrated to hamper muscle protein synthesis and increase the expression of genes associated with defective muscle maintenance such as Mstn and Muscle atrophy F-box (MAFbx) (Petersen et al., 2007). Indeed, direct exposure of myotubes to sub-maximal concentrations of H2O2 also resulted in a significant induction of both Mstn (Figure 4A) and MAFbx (Figure 4B), while the production and release of IGF-1, a potent driver of protein synthesis and myogenesis (Florini, Ewton & Coolican, 1996), were concomitantly suppressed (Figure 4C-E). Like that of H2O2, direct exposure to CSE also suppressed the production and release of IGF-1 (Figure 4H-J), regardless of concentration. However, the expression of Mstn (Figure 4F) andMAFbx (Figure 4G) remained largely unaltered, suggesting the deleterious effects of CSE exposure on myofiber wasting may predominantly lie in suppression of IGF-1 mediated protein synthesis.