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First published online February 7, 2007

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Recruiting muscle from the reserves

IGF-1 plays a major role in the control of skeletal muscle growth and regeneration. It increases skeletal muscle mass and has been touted as a potential therapy for muscle wasting and neuromuscular diseases. Therefore, understanding the mechanisms by which IGF-1 induces muscle hypertrophy is paramount. On p. 670, Virginie Jacquemin and colleagues reveal that IGF-1 signals exclusively to myotubes and not reserve cells, and that the myotubes then recruit reserve cells by a secondary mechanism. IGF-1 treatment of myoblasts induces expression of markers characteristic of myogenic differentiation and induces activation of the MAPK and Akt kinases specifically in myotubes. The authors hypothesised that the myotubes must secrete a soluble factor responsible for reserve cell recruitment. Using neutralising antibodies, they identified this factor as interleukin 13 (IL-13) and demonstrate that its induction is mediated by the NFATc2 transcription factor. In addition to increased cell fusion, IGF-1 treatment stimulates myotube protein metabolism via Akt, which activates mTOR signalling (a key growth pathway) and inhibits Foxo1-atrogin1 protein degradation pathways. The authors speculate that therapeutic strategies directed at specific IGF-1 metabolic targets rather than reserve cell recruitment could potentially prolong the regenerative capacity of muscle.

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Related articles in JCS:

IL-13 mediates the recruitment of reserve cells for fusion during IGF-1-induced hypertrophy of human myotubes

Virginie Jacquemin, Gillian Sandra Butler-Browne, Denis Furling, and Vincent Mouly
JCS 2007 120: 670-681. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?