Response to Electrostimulation Is Impaired in Muscle Cells from Patients with Chronic Obstructive Pulmonary Disease

Among the comorbidities associated with chronic obstructive pulmonary disease (COPD), skeletal muscle weakness and atrophy are known to affect patient survival rate. In addition to muscle deconditioning, various systemic and intrinsic factors have been implicated in COPD muscle dysfunction but an im...

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Autores principales:	Matthias Catteau, Emilie Passerieux, Léo Blervaque, Farés Gouzi, Bronia Ayoub, Maurice Hayot, Pascal Pomiès
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	EPS satellite cells skeletal muscle COPD muscle weakness differentiation Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/3ae27adbf6a74e4ab3053679b808fabe
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spelling	oai:doaj.org-article:3ae27adbf6a74e4ab3053679b808fabe2021-11-25T17:10:19ZResponse to Electrostimulation Is Impaired in Muscle Cells from Patients with Chronic Obstructive Pulmonary Disease10.3390/cells101130022073-4409https://doaj.org/article/3ae27adbf6a74e4ab3053679b808fabe2021-11-01T00:00:00Zhttps://www.mdpi.com/2073-4409/10/11/3002https://doaj.org/toc/2073-4409Among the comorbidities associated with chronic obstructive pulmonary disease (COPD), skeletal muscle weakness and atrophy are known to affect patient survival rate. In addition to muscle deconditioning, various systemic and intrinsic factors have been implicated in COPD muscle dysfunction but an impaired COPD muscle adaptation to contraction has never been extensively studied. We submitted cultured myotubes from nine healthy subjects and nine patients with COPD to an endurance-type protocol of electrical pulse stimulation (EPS). EPS induced a decrease in the diameter, covered surface and expression of MHC1 in COPD myotubes. Although the expression of protein degradation markers was not affected, expression of the protein synthesis marker mTOR was not induced in COPD compared to healthy myotubes after EPS. The expression of the differentiation markers p16<sup>INK4a</sup> and p21 was impaired, while expression of Myf5 and MyoD tended to be affected in COPD muscle cells in response to EPS. The expression of mitochondrial biogenesis markers PGC1α and MFN2 was affected and expression of TFAM and COX1 tended to be reduced in COPD compared to healthy myotubes upon EPS. Lipid peroxidation was increased and the expression of the antioxidant enzymes SOD2 and GPx4 was affected in COPD compared to healthy myotubes in response to EPS. Thus, we provide evidence of an impaired response of COPD muscle cells to contraction, which might be involved in the muscle weakness observed in patients with COPD.Matthias CatteauEmilie PasserieuxLéo BlervaqueFarés GouziBronia AyoubMaurice HayotPascal PomièsMDPI AGarticleEPSsatellite cellsskeletal muscleCOPDmuscle weaknessdifferentiationBiology (General)QH301-705.5ENCells, Vol 10, Iss 3002, p 3002 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	EPS satellite cells skeletal muscle COPD muscle weakness differentiation Biology (General) QH301-705.5
spellingShingle	EPS satellite cells skeletal muscle COPD muscle weakness differentiation Biology (General) QH301-705.5 Matthias Catteau Emilie Passerieux Léo Blervaque Farés Gouzi Bronia Ayoub Maurice Hayot Pascal Pomiès Response to Electrostimulation Is Impaired in Muscle Cells from Patients with Chronic Obstructive Pulmonary Disease
description	Among the comorbidities associated with chronic obstructive pulmonary disease (COPD), skeletal muscle weakness and atrophy are known to affect patient survival rate. In addition to muscle deconditioning, various systemic and intrinsic factors have been implicated in COPD muscle dysfunction but an impaired COPD muscle adaptation to contraction has never been extensively studied. We submitted cultured myotubes from nine healthy subjects and nine patients with COPD to an endurance-type protocol of electrical pulse stimulation (EPS). EPS induced a decrease in the diameter, covered surface and expression of MHC1 in COPD myotubes. Although the expression of protein degradation markers was not affected, expression of the protein synthesis marker mTOR was not induced in COPD compared to healthy myotubes after EPS. The expression of the differentiation markers p16<sup>INK4a</sup> and p21 was impaired, while expression of Myf5 and MyoD tended to be affected in COPD muscle cells in response to EPS. The expression of mitochondrial biogenesis markers PGC1α and MFN2 was affected and expression of TFAM and COX1 tended to be reduced in COPD compared to healthy myotubes upon EPS. Lipid peroxidation was increased and the expression of the antioxidant enzymes SOD2 and GPx4 was affected in COPD compared to healthy myotubes in response to EPS. Thus, we provide evidence of an impaired response of COPD muscle cells to contraction, which might be involved in the muscle weakness observed in patients with COPD.
format	article
author	Matthias Catteau Emilie Passerieux Léo Blervaque Farés Gouzi Bronia Ayoub Maurice Hayot Pascal Pomiès
author_facet	Matthias Catteau Emilie Passerieux Léo Blervaque Farés Gouzi Bronia Ayoub Maurice Hayot Pascal Pomiès
author_sort	Matthias Catteau
title	Response to Electrostimulation Is Impaired in Muscle Cells from Patients with Chronic Obstructive Pulmonary Disease
title_short	Response to Electrostimulation Is Impaired in Muscle Cells from Patients with Chronic Obstructive Pulmonary Disease
title_full	Response to Electrostimulation Is Impaired in Muscle Cells from Patients with Chronic Obstructive Pulmonary Disease
title_fullStr	Response to Electrostimulation Is Impaired in Muscle Cells from Patients with Chronic Obstructive Pulmonary Disease
title_full_unstemmed	Response to Electrostimulation Is Impaired in Muscle Cells from Patients with Chronic Obstructive Pulmonary Disease
title_sort	response to electrostimulation is impaired in muscle cells from patients with chronic obstructive pulmonary disease
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/3ae27adbf6a74e4ab3053679b808fabe
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Response to Electrostimulation Is Impaired in Muscle Cells from Patients with Chronic Obstructive Pulmonary Disease

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