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Analyses of the differentiation potential of satellite cells from myoD-/-, mdx, and PMP22 C22 mice
Authors:Marion?M?Schuierer  author-information"  >  author-information__contact u-icon-before"  >  mailto:marion.schuierer@klinik.uni-r.de"   title="  marion.schuierer@klinik.uni-r.de"   itemprop="  email"   data-track="  click"   data-track-action="  Email author"   data-track-label="  "  >Email author,Christopher?J?Mann,Heidi?Bildsoe,Clare?Huxley,Simon?M?Hughes
Affiliation:(1) Insitute of Pathology, Medical School of the University of Regensburg, Franz-Josef-Strauss-Allee 11, 93053 Regensburg, Germany;(2) Division of Biomedical Sciences, and Clinical Sciences Centre, Imperial College School of Science, Technology and Medicine, London, UK;(3) MRC Centre for Developmental Neurobiology and Randall Division for Cell and Molecular Biophysics, Guy's Campus, King's College, London, UK
Abstract:

Background  

Sporadic and sometimes contradictory studies have indicated changes in satellite cell behaviour associated with the progressive nature of human Duchenne muscular dystrophy (DMD). Satellite cell proliferation and number are reportedly altered in DMD and the mdx mouse model. We recently found that satellite cells in MSVski transgenic mice, a muscle hypertrophy model showing progressive muscle degeneration, display a severe ageing-related differentiation defect in vitro. We tested the hypothesis that similar changes contribute to the gradual loss of muscle function with age in mdx and PMP22 mice, a model of human motor and sensory neuropathy type 1A (HMSN1A).
Keywords:
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