Maged1, a new regulator of skeletal myogenic differentiation and muscle regenerationReport as inadecuate




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BMC Cell Biology

, 11:57

First Online: 20 July 2010Received: 10 May 2010Accepted: 20 July 2010

Abstract

BackgroundIn 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.

ResultsWe 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 p21, defective cell cycle exit and impaired myotube maturation. In vivo, this defect results in delayed regeneration of injured muscle.

ConclusionsThese data demonstrate for the first time that Maged1 is an important factor required for proper skeletal myoblast differentiation and muscle healing.

Electronic supplementary materialThe online version of this article doi:10.1186-1471-2121-11-57 contains supplementary material, which is available to authorized users.

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Author: Tuan HN Nguyen - Mathieu JM Bertrand - Christiane Sterpin - Younes Achouri - Olivier RY De Backer

Source: https://link.springer.com/article/10.1186/1471-2121-11-57







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