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.