Hypertrophy and atrophy inversely regulate Caveolin-3 expression in myoblasts

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• 作者：Aless ; ro Fanzani ; Antonio Musarò ; Elena Stoppani ; Roberta Giuliani ; Francesca Colombo ; Augusto Preti ; Sergio Marchesini
• 关键词：Caveolin 3 ; Hypertrophy ; AKT ; Igf-1 ; Vasopressin ; Atrophy ; Starvation ; Dexamethasone
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2007
• 出版时间：25 May 2007
• 年：2007
• 卷：357
• 期：1
• 页码：314-318
• 全文大小：413 K

文摘

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 Arg⁸-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.