Maged1, a new regulator of skeletal myogenic differentiation and muscle regeneration.

BMC Cell Biology
Tuan NguyenOlivier De Backer

Abstract

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.

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Citations

Jan 10, 2013·PLoS Genetics·Gina CalabreseCharles R Farber
Feb 7, 2012·Gene·Jason Russell Bush, Rachel Wevrick
Mar 8, 2011·Bioorganic & Medicinal Chemistry Letters·Michael SchnürchMarko D Mihovilovic
Mar 8, 2016·Asian-Australasian Journal of Animal Sciences·Md ShahjahanJie Wen
Aug 15, 2015·The American Journal of Pathology·Mei LiuChuanjun Wen
Oct 27, 2016·Tumour Biology : the Journal of the International Society for Oncodevelopmental Biology and Medicine·Ge ZhangXiaoying Xue
Jul 21, 2016·Human Molecular Genetics·Ain A KamaludinRachel Wevrick
Sep 15, 2020·The Journal of Biological Chemistry·Rebecca R Florke GeePatrick Ryan Potts

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Methods Mentioned

BETA
biopsies
PCR
transfect
FACS
Assay
transfection
Protein Assay

Software Mentioned

MATLAB
Primer Express

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