Impaired calcium signaling in muscle fibers from intercostal and foot skeletal muscle in a cigarette smoke-induced mouse model of COPD: E-C Coupling Dysfunction in COPD
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Introduction Respiratory and locomotor skeletal muscle dysfunction are common findings in chronic obstructive pulmonary disease (COPD); however, the mechanisms that cause muscle impairment in COPD are unclear. Because Ca2+ signaling in excitation–contraction (E-C) coupling is important for muscle activity, we hypothesized that Ca2+ dysregulation could contribute to muscle dysfunction in COPD. Methods Intercostal and flexor digitorum brevis muscles from control and cigarette smoke-exposed mice were investigated. We used single cell Ca2+ imaging and Western blot assays to assess Ca2+ signals and E-C coupling proteins. Results We found impaired Ca2+ signals in muscle fibers from both muscle types, without significant changes in releasable Ca2+ or in the expression levels of E-C coupling proteins. Conclusions Ca2+ dysregulation may contribute or accompany respiratory and locomotor muscle dysfunction in COPD. These findings are of significance to the understanding of the pathophysiological course of COPD in respiratory and locomotor muscles. Muscle Nerve 56: 282–291, 2017
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Two studies in CS-exposed mice evidenced impaired calcium signaling, notably decreased sarcoplasmic reticulum calcium uptake.
“Two other studies performed in CS-exposed mice evidenced impaired calcium signaling, notably a decreased sarcoplasmic reticulum calcium uptake [141,142].”
From Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting (2023) · cites this paper as [141]
The Results report impaired calcium transients in muscle fibers from cigarette smoke-exposed mice. They do not report decreased sarcoplasmic reticulum calcium uptake: the Results found no significant change in transient decay or releasable calcium, and the Discussion describes calcium stores as intact. This verdict concerns only the cited Robison et al. study, not the other study cited in the sentence. (LLM, conf=0.89)
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Hood, D. A., Tryon, L. D., Carter, H. N., Kim, Y., & Chen, C. C. W. (2016) · Biochemical Journal · doi:10.1042/bcj20160009 · Cited by 159 · cited 1× · see citing works
“, Ca(21) transients elicited by trains of action potential during muscle activity) regulate cell survival by promoting mitochondria bioenergetics.(51,52) We hypothesize that depressed Ca(21) transients, as observed in muscle from cigarette-exposed mice, could contribute to muscle atrophy by affecting cell survival/dea…”
BackgroundRole of Autophagy in COPD Skeletal Muscle Dysfunction
Hussain, S. N. A., & Sandri, M. (2013) · Journal of Applied Physiology · doi:10.1152/japplphysiol.00893.2012 · Cited by 77 · see citing works
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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
“Two other studies performed in CS-exposed mice evidenced impaired calcium signaling, notably a decreased sarcoplasmic reticulum calcium uptake [141,142].”
- Authors
- Robison, P., Sussan, T. E., Chen, H., Biswal, S., Schneider, M. F., & Hernández-Ochoa, E. O.
- Affiliations
- University of Maryland, Baltimore (US)
- Johns Hopkins University (US)
- Department of Biochemistry and Molecular Biology; University of Maryland School of Medicine; 108 N. Greene Street Baltimore Maryland 21201 USA
- Venue
- Muscle & Nerve
- Publisher
- Wiley
- Published
- 2017-02-13
- Volume
- 56
- Issue
- 2
- Pages
- 282-291
- ISSN
- 0148-639X (ISSN-L)
- PMC
- PMC5426995
- OpenAlex
- W2551557276
- Cited by
- 14
- References
- 3
- Citations by year
- 2025: 1 · 2023: 5 · 2022: 2 · 2021: 1 · 2020: 1 · 2019: 1 · 2018: 2 · 2017: 1
- FWCI
- 0.69
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Muscle & Nerve (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NIH (R37-AR055099, T32-AR007592)
- FAMRI
- 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 › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Keywords
- chronic obstructive pulmonary disease, cigarette smoke, calcium signaling, excitation-contraction coupling, skeletal muscle dysfunction, intercostal muscles, flexor digitorum brevis, locomotor muscles, respiratory muscles, mouse model
- MeSH terms
- Action Potentials, Air Pollutants, Animals, Calcium, Calmodulin, Disease Models, Animal, Foot, Gene Expression Regulation, Locomotion, Male, Mice, Inbred C57BL, Muscle Contraction, S100 Proteins, Smoking, Muscle Fibers, Skeletal, Ryanodine Receptor Calcium Release Channel, Calcium Signaling, Pulmonary Disease, Chronic Obstructive, Mice
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