Respiratory Research | |
Regenerative defect in vastus lateralis muscle of patients with chronic obstructive pulmonary disease | |
Research | |
Marie-Ève Paré1  Marie-Eve Thériault1  Bruno B Lemire1  François Maltais1  Richard Debigaré1  | |
[1] Centre de recherche Institut universitaire de cardiologie et de pneumologie de Québec, Université Laval, G1V 4G5, Québec, QC, Canada; | |
关键词: Satellite cells; COPD; Muscle; Regeneration; Atrophy; | |
DOI : 10.1186/1465-9921-15-35 | |
received in 2013-11-01, accepted in 2014-03-10, 发布年份 2014 | |
来源: Springer | |
【 摘 要 】
BackgroundImpaired skeletal muscle regeneration could contribute to the progression of muscle atrophy in patients with chronic obstructive pulmonary disease (COPD).MethodsSatellite cells and myogenesis-related proteins were compared between healthy subjects and patients with COPD, with or without muscle atrophy. Satellite cells were isolated and cultured to assess their proliferative and differentiation aptitudes.ResultsAlthough satellite cell numbers in muscle samples were similar between groups, the proportion of muscle fibers with central nuclei was increased in COPD. In muscle homogenates, increased expression of MyoD and decreased expression of myogenin and MRF4 were observed in COPD. In cultured satellite cells of patients with COPD, increased protein content was observed for Pax7, Myf5 (proliferation phase) and myogenin (differentiation phase) while myosin heavy chain protein content was significantly lower during differentiation.ConclusionIn COPD, the number of central nuclei was increased in muscle fibers suggesting a greater number of attempts to regenerate muscle tissue than in healthy subjects. Myogenesis signaling was also altered in muscle homogenates in patients with COPD and there was a profound reduction in the differentiation potential in this population as indicated by a reduced ability to incorporate myosin heavy chain into newly formed myotubes. Collectively, these results indicate that skeletal muscle regenerative capacity termination is impaired in COPD and could contribute to the progression of muscle atrophy progression in this population.
【 授权许可】
Unknown
© Thériault et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
【 预 览 】
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