ArticlePloS one2015
ROS Production via P2Y1-PKC-NOX2 Is Triggered by Extracellular ATP after Electrical Stimulation of Skeletal Muscle Cells.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed.
- Systems modelling of mitochondrial dynamics in different exercise regimes.The Journal of physiology · 2026Article
- Traditional Health Practices May Promote Nrf2 Activation Similar to Exercise.International journal of molecular sciences · 2025Review
- Redox Homeostasis in Metabolic Syndrome and Type II Diabetes: Role of Skeletal Muscle and Impact of Gold-Standard Treatments.International journal of molecular sciences · 2025Review
- Metformin suppresses the mitochondrial and transcriptional response to exercise, revealing a conserved BCL6B-associated angiogenic program.Journal of applied physiology (Bethesda, Md. : 1985) · 2025Article
- Purine-based infochemicals and immunometabolites: a comparative review of emerging signaling pathways in plants and animals.FEMS microbiology reviews · 2025Review
- The sodium/ascorbic acid co-transporter SVCT2 distributes in a striated membrane-enriched domain at the M-band level in slow-twitch skeletal muscle fibers.Biological research · 2024Article
- Resistance training does not increase myocellular garbage dumps: A pilot study on lipofuscin in skeletal muscle fibers of resistance trained young men.Physiological reports · 2024Article
- Extracellular purines in lung endothelial permeability and pulmonary diseases.Frontiers in physiology · 2024Review
- Neuroinflammation in the Evolution of Motor Function in Stroke and Trauma Patients: Treatment and Potential Biomarkers.Current issues in molecular biology · 2023Review
- Energy (and Reactive Oxygen Species Generation) Saving Distribution of Mitochondria for the Activation of ATP Production in Skeletal Muscle.Antioxidants (Basel, Switzerland) · 2023Review
- Oxidative Stress in Type 2 Diabetes: Impacts from Pathogenesis to Lifestyle Modifications.Current issues in molecular biology · 2023Review
- Gap Junctions and Connexins in Microglia-Related Oxidative Stress and Neuroinflammation: Perspectives for Drug Discovery.Biomolecules · 2023Review
- Fibroblast growth factor 21 is expressed and secreted from skeletal muscle following electrical stimulationFrontiers in endocrinology · 2023Article
- Article
- 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
- Redox signaling regulates skeletal muscle remodeling in response to exercise and prolonged inactivity.Redox biology · 2022Review
- Oxidative Stress, Inflammation and Connexin Hemichannels in Muscular Dystrophies.Biomedicines · 2022Review
- Understanding Reactive Oxygen Species in Bone Regeneration: A Glance at Potential Therapeutics and Bioengineering Applications.Frontiers in bioengineering and biotechnology · 2022Review
- Purinergic signaling in the modulation of redox biology.Redox biology · 2021Review
- Genetically Encoded Biosensors to Monitor Intracellular Reactive Oxygen and Nitrogen Species and Glutathione Redox Potential in Skeletal Muscle Cells.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During exercise, skeletal muscle produces reactive oxygen species (ROS) via NADPH oxidase (NOX2) while inducing cellular adaptations associated with contractile activity. The signals involved in this mechanism are still a matter of study. ATP is released from skeletal muscle during electrical stimulation and can autocrinely signal through purinergic receptors; we searched for an influence of this signal in ROS production. The aim of this work was to characterize ROS production induced by electrical stimulation and extracellular ATP. ROS production was measured using two alternative probes; chloromethyl-2,7- dichlorodihydrofluorescein diacetate or electroporation to express the hydrogen peroxide-sensitive protein Hyper. Electrical stimulation (ES) triggered a transient ROS increase in muscle fibers which was mimicked by extracellular ATP and was prevented by both carbenoxolone and suramin; antagonists of pannexin channel and purinergic receptors respectively. In addition, transient ROS increase was prevented by apyrase, an ecto-nucleotidase. MRS2365, a P2Y1 receptor agonist, induced a large signal while UTPyS (P2Y2 agonist) elicited a much smaller signal, similar to the one seen when using ATP plus MRS2179, an antagonist of P2Y1. Protein kinase C (PKC) inhibitors also blocked ES-induced ROS production. Our results indicate that physiological levels of electrical stimulation induce ROS production in skeletal muscle cells through release of extracellular ATP and activation of P2Y1 receptors. Use of selective NOX2 and PKC inhibitors suggests that ROS production induced by ES or extracellular ATP is mediated by NOX2 activated by PKC.
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