Background: Impaired skeletal muscle regeneration could contribute to the progression of muscle atrophy in\npatients with chronic obstructive pulmonary disease (COPD).\nMethods: Satellite cells and myogenesis-related proteins were compared between healthy subjects and patients\nwith COPD, with or without muscle atrophy. Satellite cells were isolated and cultured to assess their proliferative\nand differentiation aptitudes.\nResults: Although satellite cell numbers in muscle samples were similar between groups, the proportion of muscle\nfibers with central nuclei was increased in COPD. In muscle homogenates, increased expression of MyoD and\ndecreased expression of myogenin and MRF4 were observed in COPD. In cultured satellite cells of patients with\nCOPD, increased protein content was observed for Pax7, Myf5 (proliferation phase) and myogenin (differentiation\nphase) while myosin heavy chain protein content was significantly lower during differentiation.\nConclusion: In COPD, the number of central nuclei was increased in muscle fibers suggesting a greater number of\nattempts to regenerate muscle tissue than in healthy subjects. Myogenesis signaling was also altered in muscle\nhomogenates in patients with COPD and there was a profound reduction in the differentiation potential in this\npopulation as indicated by a reduced ability to incorporate myosin heavy chain into newly formed myotubes.\nCollectively, these results indicate that skeletal muscle regenerative capacity termination is impaired in COPD and\ncould contribute to the progression of muscle atrophy progression in this population
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