Abstract：
:Insulin-like growth factor-1 (IGF-1) has been shown to induce skeletal muscle hypertrophy, to prevent the loss of muscle mass with ageing and to improve the muscle phenotype of dystrophic mice. We previously developed a model of IGF-1-induced hypertrophy of human myotubes, in which hypertrophy was not only characterized by an increase in myotube size and myosin content but also by an increased recruitment of reserve cells for fusion. Here, we describe a new mechanism of IGF-1-induced hypertrophy by demonstrating that IGF-1 signals exclusively to myotubes but not to reserve cells, leading, under the control of the transcription factor NFATc2, to the secretion of IL-13 that will secondly recruit reserve cells for differentiation and fusion. In addition, we show that IGF-1 also signals to myotubes to stimulate protein metabolism via Akt by (1) activating the mTOR-p70S6K-S6 pathway and inhibiting GSK-3beta, both involved in the control of protein translation, and (2) inhibiting the Foxo1-atrogin-1 protein degradation pathway.
journal_name
J Cell Scijournal_title
Journal of cell scienceauthors
Jacquemin V,Butler-Browne GS,Furling D,Mouly Vdoi
10.1242/jcs.03371subject
Has Abstractpub_date
2007-02-15 00:00:00pages
670-81issue
Pt 4eissn
0021-9533issn
1477-9137pii
jcs.03371journal_volume
120pub_type
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