In mammals, several evidences have demonstrated the important role of Myostatin (MSTN) in regulating muscle mass and identified the transcription factor FoxO1 as a key regulator of its gene expression during atrophy. However in trout, food deprivation leads to muscle atrophy without an increase of the expression of mstn genes in the muscle. We therefore studied the relationship between FoxO1 activity and the expression of both mstn genes (mstn1a and mstn1b) in primary culture of trout myotubes. To this aim, two complementary studies were undertaken. In the former, FoxO1 protein activity was modified with IGF1 treatment and the consequences on the expression of both mstn genes were monitored. In the second experiment, the expression of both studied genes was modified with GH treatment and the activation of FoxO1 protein was investigated. We found that IGF1 induced the phosphorylation of FoxO1 and FoxO4. Moreover, under IGF1 stimulation FoxO1 was no longer localized in the nucleus indicating that this growth factor inhibited FoxO1 activity. However, IGF1 treatment had no effect on mstn1a and mstn1b expression suggesting that FoxO1 would not regulate the expression of mstn genes in trout myotubes. Furthermore, the treatment of myotubes with Growth Hormone (GH) decreased both mstn gene expression but has no effect on the phosphorylation of FoxO1, FoxO3 and FoxO4 nor on the nuclear translocation of FoxO1. Altogether, our results showed that mstn1a and mstn1b expression were not associated with FoxO activity indicating that FoxO1 is likely not a key regulator of mstn genes in trout myotubes.
- Copyright © 2011, American Journal of Physiology - Regulatory, Integrative and Comparative Physiology