Maged1, a new regulator of skeletal myogenic differentiation and muscle regeneration
1 URPHYM (Unité de Recherche en Physiologie Moléculaire), NARILIS (Namur Research Institute for Life Sciences), FUNDP school of Medicine, University of Namur, 21 rue de Bruxelles, Namur B-5000, Belgium
2 Molecular Signaling and Cell Death Unit, Department for Molecular Biomedical Research, VIB, 9052 Ghent, Belgium
3 Department of Biomedical Molecular Biology, Ghent University, 9052 Ghent, Belgium
4 Christian de Duve Institute of Cellular Pathology, Université Catholique de Louvain (UCL), Avenue Hippocrate 75, Brussels B-1200, Belgium
Citation and License
BMC Cell Biology 2010, 11:57 doi:10.1186/1471-2121-11-57Published: 20 July 2010
In normal adult skeletal muscle, cell turnover is very slow. However, after an acute lesion or in chronic pathological conditions, such as primary myopathies, muscle stem cells, called satellite cells, are induced to proliferate, then withdraw definitively from the cell cycle and fuse to reconstitute functional myofibers.
We show that Maged1 is expressed at very low levels in normal adult muscle but is strongly induced after injury, during the early phase of myoblast differentiation. By comparing in vitro differentiation of myoblasts derived from wild-type or Maged1 knockout mice, we observed that Maged1 deficiency results in reduced levels of p21CIP1/WAF1, defective cell cycle exit and impaired myotube maturation. In vivo, this defect results in delayed regeneration of injured muscle.
These data demonstrate for the first time that Maged1 is an important factor required for proper skeletal myoblast differentiation and muscle healing.