Oxidative Stress Regulates Autophagy in Cultured Muscle Cells of Patients with Chronic Obstructive Pulmonary Disease
Open accessAbstract
The proteolytic autophagy pathway is enhanced in the lower limb muscles of patients with chronic obstructive pulmonary disease (COPD). Reactive oxygen species (ROS) have been shown to regulate autophagy in the skeletal muscles, but the role of oxidative stress in the muscle autophagy of patients with COPD is unknown. We used cultured myoblasts and myotubes from the quadriceps of eight healthy subjects and twelve patients with COPD (FEV1% predicted: 102.0% and 32.0%, respectively; p < 0.0001). We compared the autophagosome formation, the expression of autophagy markers, and the autophagic flux in healthy subjects and the patients with COPD, and we evaluated the effects of the 3-methyladenine (3-MA) autophagy inhibitor on the atrophy of COPD myotubes. Autophagy was also assessed in COPD myotubes treated with an antioxidant molecule, ascorbic acid. Autophagosome formation was increased in COPD myoblasts and myotubes (p = 0.011; p < 0.001), and the LC3 2/LC3 1 ratio (p = 0.002), SQSTM1 mRNA and protein expression (p = 0.023; p = 0.007), BNIP3 expression (p = 0.031), and autophagic flux (p = 0.002) were higher in COPD myoblasts. Inhibition of autophagy with 3-MA increased the COPD myotube diameter (p < 0.001) to a level similar to the diameter of healthy subject myotubes. Treatment of COPD myotubes with ascorbic acid decreased ROS concentration (p < 0.001), ROS-induced protein carbonylation (p = 0.019), the LC3 2/LC3 1 ratio (p = 0.037), the expression of SQSTM1 (p < 0.001) and BNIP3 (p < 0.001), and increased the COPD myotube diameter (p < 0.001). Thus, autophagy signaling is enhanced in cultured COPD muscle cells. Furthermore, the oxidative stress level contributes to the regulation of autophagy, which is involved in the atrophy of COPD myotubes in vitro.
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An increased LC3BII/LC3BI ratio and p62/SQSTM1 protein levels were also reported in cultured myoblasts from COPD patients compared to healthy subjects.
“An increased LC3BII/LC3BI ratio and p62/SQSTM1 protein levels were also reported in cultured myoblasts from COPD patients compared to healthy subjects [184].”
From Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting (2023) · cites this paper as [184]
Increased autophagy is directly linked to oxidative stress, as treatment with an antioxidant molecule decreased autophagy levels in cultured myotubes.
“Moreover, it has also been reported that increased autophagy was directly linked to oxidative stress, as treatment with an antioxidant molecule decreased autophagy levels in cultured myotubes [184].”
From Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting (2023) · cites this paper as [184]
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Cites
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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
“Moreover, it has also been reported that increased autophagy was directly linked to oxidative stress, as treatment with an antioxidant molecule decreased autophagy levels in cultured myotubes [184].”
BackgroundSelf-citation
- Authors
- Gouzi, F., Blaquière, M., Catteau, M., Bughin, F., Maury, J., Passerieux, E., Ayoub, B., Mercier, J., Hayot, M., & Pomiès, P.
- Affiliations
- PhyMedExp, University of Montpellier, INSERM, CNRS Montpellier France
- Centre National de la Recherche Scientifique (FR)
- Corresponding author
- Pomiès, Pascal
- ORCID
- Venue
- Journal of Cellular Physiology
- Publisher
- Wiley
- Published
- 2018-06-26
- Volume
- 233
- Issue
- 12
- Pages
- 9629-9639
- ISSN
- 0021-9541 (ISSN-L)
- 1097-4652
- OpenAlex
- W2809958583
- Cited by
- 29
- References
- 1
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 2 · 2023: 5 · 2022: 4 · 2021: 5 · 2020: 5 · 2019: 2 · 2018: 2
- FWCI
- 1.25
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Cellular Physiology (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- Funders
- CHRU of Montpellier (PHRC (AREB-1))
- Apard (Association Pour l’Assistance et la Réhabilitation à Domicile)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Keywords
- chronic obstructive pulmonary disease, autophagy, oxidative stress, reactive oxygen species, skeletal muscle atrophy, myotubes, myoblasts, autophagosome formation, autophagic flux, LC3, p62, BNIP3, 3-methyladenine, vitamin C, protein carbonylation, lower limb muscles, quadriceps
- MeSH terms
- Adenine, Aged, Ascorbic Acid, Autophagy, Cells, Cultured, Female, Humans, Male, Microtubule-Associated Proteins, Middle Aged, Muscular Atrophy, Phagosomes, Biomarkers, Oxidative Stress, Muscle Fibers, Skeletal, Pulmonary Disease, Chronic Obstructive, Muscle Cells, Myoblasts
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