ArticleAmerican journal of physiology. Cell physiology2010
Excitation-contraction coupling alterations in mdx and utrophin/dystrophin double knockout mice: a comparative study.
Article in American journal of physiology. Cell physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 37 citations in OpenAlex.
- Proteomic profiling of impaired excitation-contraction coupling and abnormal calcium handling in muscular dystrophy.Proteomics · 2022Review
- Postdevelopmental knockout of Orai1 improves muscle pathology in a mouse model of Duchenne muscular dystrophy.The Journal of general physiology · 2022Article
- Complexity of skeletal muscle degeneration: multi-systems pathophysiology and organ crosstalk in dystrophinopathy.Pflugers Archiv : European journal of physiology · 2021Review
- Loss of dysferlin or myoferlin results in differential defects in excitation-contraction coupling in mouse skeletal muscle.Scientific reports · 2021Article
- Abnormal Calcium Handling in Duchenne Muscular Dystrophy: Mechanisms and Potential Therapies.Frontiers in physiology · 2021Review
- Development of a high-throughput screen to identify small molecule enhancers of sarcospan for the treatment of Duchenne muscular dystrophy.Skeletal muscle · 2019Article
- Muscle dysfunction in a zebrafish model of Duchenne muscular dystrophy.Physiological genomics · 2016Article
- Attenuated Ca(2+) release in a mouse model of limb girdle muscular dystrophy 2A.Skeletal muscle · 2016Article
- Alternating bipolar field stimulation identifies muscle fibers with defective excitability but maintained local Ca(2+) signals and contraction.Skeletal muscle · 2016Article
- The role of proteases in excitation-contraction coupling failure in muscular dystrophy.American journal of physiology. Cell physiology · 2015Article
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- Perturbations in intracellular Ca2+ handling in skeletal muscle in the G93A*SOD1 mouse model of amyotrophic lateral sclerosis.American journal of physiology. Cell physiology · 2014Article
- Triadopathies: an emerging class of skeletal muscle diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2014Review
- New insights on contraction efficiency in patients with Duchenne muscular dystrophy.Journal of applied physiology (Bethesda, Md. : 1985) · 2014Article
- Myofibrillar misalignment correlated to triad disappearance of mdx mouse gastrocnemius muscle probed by SHG microscopy.Biomedical optics express · 2014Article
- Action potential-evoked calcium release is impaired in single skeletal muscle fibers from heart failure patients.PloS one · 2014Article
- Whole body periodic acceleration is an effective therapy to ameliorate muscular dystrophy in mdx mice.PloS one · 2014Article
- Increased sarcolipin expression and decreased sarco(endo)plasmic reticulum Ca2+ uptake in skeletal muscles of mouse models of Duchenne muscular dystrophy.Journal of muscle research and cell motility · 2013Article
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3 authors.
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Abstract
The double knockout mouse for utrophin and dystrophin (utr(-/-)/mdx) has been proposed to be a better model of Duchenne Muscular Dystrophy (DMD) than the mdx mouse because the former displays more similar muscle pathology to that of the DMD patients. In this paper the properties of action potentials (APs) and Ca(2+) transients elicited by single and repetitive stimulation were studied to understand the excitation-contraction (EC) coupling alterations observed in muscle fibers from mdx and utr(-/-)/mdx mice. Based on the comparison of the AP durations with those of fibers from wild-type (WT) mice, fibers from both mdx and utr(-/-)/mdx mice could be divided in two groups: fibers with WT-like APs (group 1) and fibers with significantly longer APs (group 2). Although the proportion of fibers in group 2 was larger in utr(-/-)/mdx (36%) than in mdx mice (27%), the Ca(2+) release elicited by single stimulation was found to be similarly depressed (32-38%) in utr(-/-)/mdx and mdx fibers compared with WT counterparts regardless of the fiber's group. Stimulation at 100 Hz revealed that, with the exception of those from utr(-/-)/mdx mice, group 1 fibers were able to sustain Ca(2+) release for longer than group 2 fibers, which displayed an abrupt limitation even at the onset of the train. The differences in behavior between fibers in groups 1 and 2 became almost unnoticeable at 50 Hz stimulation. In general, fibers from utr(-/-)/mdx mice seem to display more persistent alterations in the EC coupling than those observed in the mdx model.
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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.