Impaired muscle regeneration and myoblast differentiation in mice with a muscle-specific KO of IGF-IR
Version of Record online: 10 MAY 2010
Copyright © 2010 Wiley-Liss, Inc.
Journal of Cellular Physiology
Volume 225, Issue 1, pages 1–6, October 2010
How to Cite
Heron-Milhavet, L., Mamaeva, D., LeRoith, D., Lamb, N. J. and Fernandez, A. (2010), Impaired muscle regeneration and myoblast differentiation in mice with a muscle-specific KO of IGF-IR. J. Cell. Physiol., 225: 1–6. doi: 10.1002/jcp.22218
- Issue online: 15 JUL 2010
- Version of Record online: 10 MAY 2010
- Manuscript Accepted: 14 APR 2010
- Manuscript Received: 27 JAN 2010
- Association pour la Recherche contre le Cancer. Grant Number: 3976
- Association Française contre les Myopathies
IGF-I and its receptor IGF-IR are seen as critical effectors of muscle hypertrophy, a notion recently questioned. Using MKR transgenic mice that express a dominant negative IGF-IR only in skeletal muscle, we have examined the role of the IGF-IR signaling in differentiation and repair of muscle fibers after damage-induced muscle regeneration. This process is impaired in MKR muscle, with incomplete regeneration, persistence of infiltrating cells and sustained expression of differentiation markers. Analysis of MKR and WT muscle-derived progenitor stem cells and myoblasts showed twice as many such cells in MKR muscle and an incomplete in vitro differentiation, that is, despite similar levels of myogenin expression, the level of fusion of MKR myoblasts was significantly reduced in comparison to WT myoblasts. These data show IGF-IR signaling is not only required at early hyperplasia stages of muscle differentiation, but also for late stages of myofiber maturation and hypertrophy. J. Cell. Physiol. 225: 1–6, 2010. © 2010 Wiley-Liss, Inc.