ArticleThe Journal of physiology2005
Effects of stretch-activated channel blockers on [Ca2+]i and muscle damage in the mdx mouse.
Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers.
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Who cites it
136 citing papers in PubMed, 263 citations in OpenAlex.
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- Mechanotransduction for Muscle Protein Synthesis via Mechanically Activated Ion Channels.Life (Basel, Switzerland) · 2023Review
- Proteomic profiling of impaired excitation-contraction coupling and abnormal calcium handling in muscular dystrophy.Proteomics · 2022Review
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- Pharmacological TRPC6 inhibition improves survival and muscle function in mice with Duchenne muscular dystrophy.JCI insight · 2022Article
- Postdevelopmental knockout of Orai1 improves muscle pathology in a mouse model of Duchenne muscular dystrophy.The Journal of general physiology · 2022Article
- The Donnan-dominated resting state of skeletal muscle fibers contributes to resilience and longevity in dystrophic fibers.The Journal of general physiology · 2022Article
- Skeletal Ryanodine Receptors Are Involved in Impaired Myogenic Differentiation in Duchenne Muscular Dystrophy Patients.International journal of molecular sciences · 2021Article
- Alteration of STIM1/Orai1-Mediated SOCE in Skeletal Muscle: Impact in Genetic Muscle Diseases and Beyond.Cells · 2021Review
- Aberrant NLRP3 Inflammasome Activation Ignites the Fire of Inflammation in Neuromuscular Diseases.International journal of molecular sciences · 2021Review
- Contraction-Induced Loss of Plasmalemmal Electrophysiological Function Is Dependent on the Dystrophin Glycoprotein Complex.Frontiers in physiology · 2021Article
- Lifespan Analysis of DystrophicFrontiers in physiology · 2021Article
- Current Pharmacological Strategies for Duchenne Muscular Dystrophy.Frontiers in cell and developmental biology · 2021Review
76 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mdx mouse lacks dystrophin and is a model of human Duchenne muscular dystrophy. Single mdx muscle fibres were isolated and subjected to a series of stretched (eccentric) contractions while measuring intracellular calcium concentration ([Ca(2+)](i)) with fluo-3 and confocal microscopy. Following the stretched contractions there was a slow rise in resting [Ca(2+)](i) and after 30 min both the [Ca(2+)](i) during a tetanus (tetanic [Ca(2+)](i)) and the tetanic force were reduced. Two blockers of stretch-activated channels, streptomycin and the spider venom toxin GsMTx4, prevented the rise of resting [Ca(2+)](i) and partially prevented the decline of tetanic [Ca(2+)](i) and force. Reducing extracellular calcium to zero also prevented the rise in resting [Ca(2+)](i) and prevented some of the decline in tetanic [Ca(2+)](i) and force. Patch-clamping experiments identified a stretch-activated channel in both wild-type and mdx myotubes which was blocked by GsMTx4. These data suggest that blockers of stretch-activated channels can ameliorate the force reduction following stretched contractions by reducing the influx of Ca(2+) into the muscle. We therefore tested whether in intact mdx mice streptomycin, added to the drinking water, was capable of reducing muscle damage. mdx mice show a period of muscle damage from 20 to 40 days of life and fibres which regenerate from this damage display central nuclei. We measured the frequency of central nuclei in control mdx mice compared to streptomycin-treated mdx mice and showed that the incidence of central nuclei was significantly reduced by streptomycin treatment. This result suggests that blockers of stretch-activated channels may protect against muscle damage in the intact mdx mouse.
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