Il-13 Mediates the Recruitment of Reserve Cells for Fusion During Igf-1-induced Hypertrophy of Human Myotubes.
From: UMR S 787, Inserm/UPMC-Paris 6, Institut de Myologie, Paris, France.
Journal of cell science
- Publish Date: Feb 2007
- ISSN: 0021-9533
- Volume: 120
- Issue: Pt 4
- Pages: 670-81
- Medium: Print
- Language: English
- Citation (JAMA): Jacquemin Virginie, Butler-Browne Gillian Sandra, Furling Denis, et al. Il-13 Mediates the Recruitment of Reserve Cells for Fusion During Igf-1-induced Hypertrophy of Human Myotubes.. J. Cell. Sci. Feb 2007;120:670-81
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.
Mesh Headings (Keywords): Cells, Cultured, Enzyme Inhibitors, Flavonoids, Humans, Hypertrophy, Imidazoles, Insulin-Like Growth Factor I, Interleukin-13, Membrane Fusion, Muscle Fibers, Pyridines
Check for Full Text / PubMed Unique Identifier (PMID): 17264150
This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.
Linked medical terms appearing on this page are added by Healia to help readers find more information and are not part of the original PubMed document.
The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.