Altered in vitro Proliferation of Mouse SOD1-G93A Skeletal Muscle Satellite Cells
Author(s) -
Raquel Manzano,
Janne M. Toivonen,
Ana Cristina Calvo,
Sara Oliván,
P. Zaragoza,
C. Rodellar,
Didier Montarras,
Rosario Osta
Publication year - 2012
Publication title -
neurodegenerative diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.98
H-Index - 57
eISSN - 1660-2862
pISSN - 1660-2854
DOI - 10.1159/000338061
Subject(s) - sod1 , amyotrophic lateral sclerosis , denervation , biology , skeletal muscle , atrophy , myocyte , medicine , motor neuron , muscle atrophy , endocrinology , microbiology and biotechnology , neuroscience , disease , spinal cord
Amyotrophic lateral sclerosis (ALS) is the most common adult-onset neurodegenerative disease characterized by ascending muscle weakness, atrophy and paralysis. Early muscle abnormalities that precede motor neuron loss in ALS may destabilize neuromuscular junctions, and we have previously demonstrated alterations in myogenic regulatory factor (MRF) expression in vivo and in the activation of myofiber-associated skeletal muscle satellite cells (SMSCs) in the mouse model of ALS (SOD1-G93A).
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