Activation of ERK by sodium tungstate induces protein synthesis and prevents protein degradation in rat L6 myotubes
FEBS Lett Available online 17 May 2014 Rafael Salto
• Activation of ERK by sodium tungstate in a skeletal muscle cell line translates.
• An increase in protein synthesis as a result of mTOR activation.
• An improvement in protein turnover in dexamethasone-treated skeletal muscle cells.
• A decrease in dexamethasone-induced protein degradation as a result of FoxO3a inhibition.
• Activation of ERK by sodium tungstate may provide a therapeutic strategy to prevent skeletal muscle atrophy.
The balance between the rates of protein synthesis and degradation in muscle is regulated by PI3K/Akt signaling. Here we addressed the effect of ERK activation by sodium tungstate on protein turnover in rat L6 myotubes. Phosphorylation of ERK by this compound increased protein synthesis by activating MTOR and prevented dexamethasone-induced protein degradation by blocking FoxO3a activity, but it did not alter Akt phosphorylation. Thus, activation of ERK by tungstate improves protein turnover in dexamethasone-treated cells. On the basis of our results, we propose that tungstate be considered an alternative to IGF-I and its analogs in the prevention of skeletal muscle atrophy.
Voir aussi :
- De nouvelles cellules souches découvertes dans les muscles
- L'ostéocalcine est une hormone anabolique pour les muscles
- Trop de leucine: néfaste pour le cœur des sportifs?
- Les muscles peuvent aussi produire de l'EPO
- Du Tadalafil pour maigrir?