ArticlePloS one2013
Electrical stimuli are anti-apoptotic in skeletal muscle via extracellular ATP. Alteration of this signal in Mdx mice is a likely cause of dystrophy.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- Effects of Electrical Muscle Stimulation on Waist Circumstance in Adults with Adbominal Obesity: A Randomized, Double-blind, Sham-Controlled Trial.JNMA; journal of the Nepal Medical AssociationTrial
- Pannexins in the musculoskeletal system: new targets for development and disease progression.Bone research · 2024Review
- Pannexin 1 dysregulation in Duchenne muscular dystrophy and its exacerbation of dystrophic features in mdx mice.Skeletal muscle · 2024Article
- Fibroblast growth factor 21 is expressed and secreted from skeletal muscle following electrical stimulationFrontiers in endocrinology · 2023Article
- Mechanical Disturbance of Osteoclasts Induces ATP Release That Leads to Protein Synthesis in Skeletal Muscle through an Akt-mTOR Signaling Pathway.International journal of molecular sciences · 2022Article
- Cardiovascular Disease in Duchenne Muscular Dystrophy: Overview and Insight Into Novel Therapeutic Targets.JACC. Basic to translational science · 2022Review
- Pannexin-1 and CaV1.1 show reciprocal interaction during excitation-contraction and excitation-transcription coupling in skeletal muscle.The Journal of general physiology · 2021Article
- Dysregulation of Calcium Handling in Duchenne Muscular Dystrophy-Associated Dilated Cardiomyopathy: Mechanisms and Experimental Therapeutic Strategies.Journal of clinical medicine · 2020Review
- Muscle function decline and mitochondria changes in middle age precede sarcopenia in mice.Aging · 2018Article
- Fast skeletal myofibers of mdx mouse, model of Duchenne muscular dystrophy, express connexin hemichannels that lead to apoptosis.Cellular and molecular life sciences : CMLS · 2016Article
- NOX2 Inhibition Impairs Early Muscle Gene Expression Induced by a Single Exercise Bout.Frontiers in physiology · 2016Article
- Dystrophin: The dead calm of a dogma.Rare diseases (Austin, Tex.) · 2016Article
- Characterization of a multiprotein complex involved in excitation-transcription coupling of skeletal muscle.Skeletal muscle · 2016Article
- P2RX7 purinoceptor: a therapeutic target for ameliorating the symptoms of duchenne muscular dystrophy.PLoS medicine · 2015Article
- The pannexins: past and present.Frontiers in physiology · 2014Review
- Cxs and Panx- hemichannels in peripheral and central chemosensing in mammals.Frontiers in cellular neuroscience · 2014Review
- Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ATP signaling has been shown to regulate gene expression in skeletal muscle and to be altered in models of muscular dystrophy. We have previously shown that in normal muscle fibers, ATP released through Pannexin1 (Panx1) channels after electrical stimulation plays a role in activating some signaling pathways related to gene expression. We searched for a possible role of ATP signaling in the dystrophy phenotype. We used muscle fibers from flexor digitorum brevis isolated from normal and mdx mice. We demonstrated that low frequency electrical stimulation has an anti-apoptotic effect in normal muscle fibers repressing the expression of Bax, Bim and PUMA. Addition of exogenous ATP to the medium has a similar effect. In dystrophic fibers, the basal levels of extracellular ATP were higher compared to normal fibers, but unlike control fibers, they do not present any ATP release after low frequency electrical stimulation, suggesting an uncoupling between electrical stimulation and ATP release in this condition. Elevated levels of Panx1 and decreased levels of Cav1.1 (dihydropyridine receptors) were found in triads fractions prepared from mdx muscles. Moreover, decreased immunoprecipitation of Cav1.1 and Panx1, suggest uncoupling of the signaling machinery. Importantly, in dystrophic fibers, exogenous ATP was pro-apoptotic, inducing the transcription of Bax, Bim and PUMA and increasing the levels of activated Bax and cytosolic cytochrome c. These evidence points to an involvement of the ATP pathway in the activation of mechanisms related with cell death in muscular dystrophy, opening new perspectives towards possible targets for pharmacological therapies.
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