| First Author | Fanzani A | Year | 2007 |
| Journal | Biochem Biophys Res Commun | Volume | 357 |
| Issue | 1 | Pages | 314-8 |
| PubMed ID | 17418092 | Mgi Jnum | J:122359 |
| Mgi Id | MGI:3714112 | Doi | 10.1016/j.bbrc.2007.03.148 |
| Citation | Fanzani A, et al. (2007) Hypertrophy and atrophy inversely regulate Caveolin-3 expression in myoblasts. Biochem Biophys Res Commun 357(1):314-8 |
| abstractText | Caveolin-3 (Cav-3) is a muscle-specific membrane protein crucial for myoblast differentiation, as loss of the protein due to mutations within the gene causes an autosomal dominant form of limb girdle muscular dystrophy 1-c. Here we show that along with p38 activity the PI3-kinase/AKT/mTOR pathway is required for proper Cav-3 up-regulation during muscle differentiation and hypertrophy, as confirmed by the marked increase of Cav-3 expression in hypertrophied C2C12 cells transfected with an activated form of AKT. Accordingly, Cav-3 expression was further increased during hypertrophy of L6C5 myoblasts treated with Arg(8)-vasopressin and in hypertrophic muscles of MLC/mIGF-1 transgenic mice. In contrast, Cav-3 expression was down-regulated in C2C12 myotubes exposed to atrophic stimuli such as starvation or treatment with dexamethasone. This study clearly suggests that Cav-3 expression is causally linked to the maturation of muscle phenotype and it is tightly regulated by hypertrophic and atrophic stimuli. |
