ArticleProceedings of the National Academy of Sciences of the United States of America2008
Dystrophic skeletal muscle fibers display alterations at the level of calcium microdomains.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- Postdevelopmental knockout of Orai1 improves muscle pathology in a mouse model of Duchenne muscular dystrophy.The Journal of general physiology · 2022Article
- Excitation-contraction coupling in mammalian skeletal muscle: Blending old and last-decade research.Frontiers in physiology · 2022Review
- Abnormal Calcium Handling in Duchenne Muscular Dystrophy: Mechanisms and Potential Therapies.Frontiers in physiology · 2021Review
- Dysregulated mitochondrial CaArchives of biochemistry and biophysics · 2019Review
- Nanospan, an alternatively spliced isoform of sarcospan, localizes to the sarcoplasmic reticulum in skeletal muscle and is absent in limb girdle muscular dystrophy 2F.Skeletal muscle · 2017Article
- Absence of physiological CaSkeletal muscle · 2017Article
- Mitochondrial Ca(2+) uptake in skeletal muscle health and disease.Science China. Life sciences · 2016Review
- Alternating bipolar field stimulation identifies muscle fibers with defective excitability but maintained local Ca(2+) signals and contraction.Skeletal muscle · 2016Article
- Attenuated Ca(2+) release in a mouse model of limb girdle muscular dystrophy 2A.Skeletal muscle · 2016Article
- Myofibrillar misalignment correlated to triad disappearance of mdx mouse gastrocnemius muscle probed by SHG microscopy.Biomedical optics express · 2014Article
- Article
- Action potential-evoked calcium release is impaired in single skeletal muscle fibers from heart failure patients.PloS one · 2014Article
- Early metabolic changes measured by 1H MRS in healthy and dystrophic muscle after injury.Journal of applied physiology (Bethesda, Md. : 1985) · 2012Article
- Leaky ryanodine receptors in β-sarcoglycan deficient mice: a potential common defect in muscular dystrophy.Skeletal muscle · 2012Article
- Sarcoplasmic reticulum Ca2+ permeation explored from the lumen side in mdx muscle fibers under voltage control.The Journal of general physiology · 2012Article
- Mitochondrial calcium uptake regulates rapid calcium transients in skeletal muscle during excitation-contraction (E-C) coupling.The Journal of biological chemistry · 2011Article
- Mitigation of muscular dystrophy in mice by SERCA overexpression in skeletal muscle.The Journal of clinical investigation · 2011Article
- Excitation-contraction coupling alterations in mdx and utrophin/dystrophin double knockout mice: a comparative study.American journal of physiology. Cell physiology · 2010Article
- Microarchitecture is severely compromised but motor protein function is preserved in dystrophic mdx skeletal muscle.Biophysical journal · 2010Article
- Hyperactive intracellular calcium signaling associated with localized mitochondrial defects in skeletal muscle of an animal model of amyotrophic lateral sclerosis.The Journal of biological chemistry · 2010Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The spatiotemporal properties of the Ca(2+)-release process in skeletal muscle fibers from normal and mdx fibers were determined using the confocal-spot detection technique. The Ca(2+) indicator OGB-5N was used to record action potential-evoked fluorescence signals at consecutive locations separated by 200 nm along multiple sarcomeres of FDB fibers loaded with 10- and 30-mM EGTA. Three-dimensional reconstructions of fluorescence transients demonstrated the existence of microdomains of increased fluorescence around the Ca(2+)-release sites in both mouse strains. The Ca(2+) microdomains in mdx fibers were regularly spaced along the fiber axis, displaying a distribution similar to that seen in normal fibers. Nevertheless, both preparations differed in that in 10-mM EGTA Ca(2+) microdomains had smaller amplitudes and were wider in mdx fibers than in controls. In addition, Ca(2+)-dependent fluorescence transients recorded at selected locations within the sarcomere of mdx muscle fibers were not only smaller, but also slower than their counterparts in normal fibers. Notably, differences in the spatial features of the Ca(2+) microdomains recorded in mdx and normal fibers, but not in the amplitude and kinetics of the Ca(2+) transients, were eliminated in 30-mM EGTA. Our results consistently demonstrate that Ca(2+)-release flux calculated from release sites in mdx fibers is uniformly impaired with respect to those normal fibers. The Ca(2+)-release reduction is consistent with that previously measured using global detection techniques.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.