Reduced myotube diameter, atrophic signalling and elevated oxidative stress in cultured satellite cells from COPD patients
Open accessAbstract
The mechanisms leading to skeletal limb muscle dysfunction in chronic obstructive pulmonary disease ( COPD ) have not been fully elucidated. Exhausted muscle regenerative capacity of satellite cells has been evocated, but the capacity of satellite cells to proliferate and differentiate properly remains unknown. Our objectives were to compare the characteristics of satellite cells derived from COPD patients and healthy individuals, in terms of proliferative and differentiation capacities, morphological phenotype and atrophy/hypertrophy signalling, and oxidative stress status. Therefore, we purified and cultivated satellite cells from progressively frozen vastus lateralis biopsies of eight COPD patients and eight healthy individuals. We examined proliferation parameters, differentiation capacities, myotube diameter, expression of atrophy/hypertrophy markers, oxidative stress damages, antioxidant enzyme expression and cell susceptibility to H 2 O 2 in cultured myoblasts and/or myotubes. Proliferation characteristics and commitment to terminal differentiation were similar in COPD patients and healthy individuals, despite impaired fusion capacities of COPD myotubes. Myotube diameter was smaller in COPD patients ( P = 0.015), and was associated with a higher expression of myostatin (myoblasts: P = 0.083; myotubes: P = 0.050) and atrogin‐1 (myoblasts: P = 0.050), and a decreased phospho‐ AKT / AKT ratio (myoblasts: P = 0.022). Protein carbonylation (myoblasts: P = 0.028; myotubes: P = 0.002) and lipid peroxidation (myotubes: P = 0.065) were higher in COPD cells, and COPD myoblasts were significantly more susceptible to oxidative stress. Thus, cultured satellite cells from COPD patients display characteristics of morphology, atrophic signalling and oxidative stress similar to those described in in vivo COPD skeletal limb muscles. We have therefore demonstrated that muscle alteration in COPD can be studied by classical in vitro cellular models.
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Increased Mn-superoxide dismutase (SOD) and Cu-Zn-SOD protein levels have been demonstrated in COPD quadriceps, whereas unchanged SOD content and decreased SOD activity have been reported in another study, and unchanged MnSOD, Cu/ZnSOD, and catalase expressions have been found in cultured COPD myoblasts and myotubes.
“For example, increased Mn-superoxide dismutase (SOD) and Cu-Zn-SOD protein levels have been demonstrated in the quadriceps [118,127], whereas unchanged SOD content and decreased SOD activity have been reported in another study [122], and unchanged MnSOD, Cu/ZnSOD, and catalase expressions in cultured COPD myoblasts and myotubes have been found [128].”
From Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting (2023) · cites this paper as [128]
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Experimental — accuracy not yet measuredSeveral studies have found increased lipofuscin accumulation in COPD quadriceps and higher levels of 4-HNE in quadriceps tissue, as well as in cultured myotubes from COPD patients.
“For example, several studies have found an increased lipofuscin accumulation in COPD quadriceps [126] and higher levels of hydroxy-2-nonenal (4-HNE) in quadriceps tissue [87,127], as well as in cultured myotubes from COPD patients [128].”
From Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting (2023) · cites this paper as [128]
The Results section reports higher measured 4-HNE levels in cultured myotubes from COPD patients than in controls, which supports the portion attributed to this paper. It describes the difference as a tendency (P = 0.065), however, so the unqualified claim of higher levels overstates the evidence. The lipofuscin and quadriceps-tissue claims have other citations. (LLM, conf=0.87)
Experimental — accuracy not yet measuredGlutathione peroxidase 1 is increased in cultured COPD myoblasts.
“Of note, we have shown an increase in glutathione peroxidase 1 in cultured COPD myoblasts [128].”
From Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting (2023) · cites this paper as [128]
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Research works printed but not linked: 40
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Cited by
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Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting
Henrot, P., Dupin, I., Schilfarth, P., Esteves, P., Blervaque, L., Zysman, M., Gouzi, F., Hayot, M., Pomiès, P., & Berger, P. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24076454 · Cited by 85 · see citing works
“tissue [87,127], as well as in cultured myotubes from COPD patients [128].”
BackgroundSelf-citationChaillou1, T., & Lanner, J. T. (2016) · The FASEB Journal · doi:10.1096/fj.201600757r · Cited by 84 · see citing works
- Authors
- Pomiès, P., Rodriguez, J., Blaquière, M., Sedraoui, S., Gouzi, F., Carnac, G., Laoudj‐Chenivesse, D., Mercier, J., Préfaut, C., & Hayot, M.
- Affiliations
- Inserm (FR)
- INSERM U‐1046 University Montpellier I University Montpellier II Montpellier France
- Corresponding author
- Pomiès, Pascal
- ORCID
- Venue
- Journal of Cellular and Molecular Medicine
- Publisher
- Wiley
- Published
- 2014-10-22
- Volume
- 19
- Issue
- 1
- Pages
- 175-186
- ISSN
- 1582-1838 (ISSN-L)
- 1582-4934
- PMC
- PMC4288361
- OpenAlex
- W1988850834
- Cited by
- 61
- References
- 0
- Citations by year
- 2026: 5 · 2025: 2 · 2024: 5 · 2023: 5 · 2022: 6 · 2021: 7 · 2020: 6 · 2019: 5 · 2018: 8 · 2017: 4 · 2016: 6 · 2015: 2
- FWCI
- 1.64
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Journal of Cellular and Molecular Medicine (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
- Life Sciences › Agricultural and Biological Sciences › Animal Science and Zoology › Meat and Animal Product Quality
- Keywords
- chronic obstructive pulmonary disease, satellite cells, skeletal muscle atrophy, myotube diameter, oxidative stress, myostatin, atrogin-1, Akt signaling, protein carbonylation, lipid peroxidation, myoblast fusion, muscle regeneration, vastus lateralis
- MeSH terms
- Aged, Cell Differentiation, Cell Fusion, Cells, Cultured, Female, Humans, Hydrogen Peroxide, Male, Middle Aged, Muscle Proteins, Muscular Atrophy, RNA, Messenger, Protein Biosynthesis, Lipid Peroxidation, Signal Transduction, Biomarkers, Case-Control Studies, Oxidative Stress, Muscle Fibers, Skeletal, Pulmonary Disease, Chronic Obstructive, Myoblasts, Satellite Cells, Skeletal Muscle, Cell Size, Cell Proliferation, Protein Carbonylation
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