ArticleProceedings of the National Academy of Sciences of the United States of America2004
A role of reactive oxygen species in apoptotic activation of volume-sensitive Cl(-) channel.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers.
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Who cites it
100 citing papers in PubMed, 233 citations in OpenAlex.
- LRRC8A: A multifaceted regulator in cancer, neurological disorders, metabolic diseases and immune modulation.Genes & diseases · 2026Review
- Excitotoxic neuronal death requires superoxide entry into neurons through volume-regulated anion channels.Science advances · 2025Article
- Cerebrospinal Fluid Biomarkers in Opioid Dependence: Evidence of Neuroimmune Activation and Ion Composition Changes, Without Alteration in Orexin-A.Addiction biology · 2025Article
- Boi-Ogi-To, a Traditional Japanese Kampo Medicine, Promotes Cellular Excretion of Chloride and Water by Activating Volume-Sensitive Outwardly Rectifying Anion Channels.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Physiology of the volume-sensitive/regulatory anion channel VSOR/VRAC: part 2: its activation mechanisms and essential roles in organic signal release.The journal of physiological sciences : JPS · 2024Review
- Physiology of the volume-sensitive/regulatory anion channel VSOR/VRAC. Part 1: from its discovery and phenotype characterization to the molecular entity identification.The journal of physiological sciences : JPS · 2024Review
- Physiological Functions of the Volume-Regulated Anion Channel VRAC/LRRC8 and the Proton-Activated Chloride Channel ASOR/TMEM206.Handbook of experimental pharmacology · 2024Article
- VRAC channel inhibition as a novel strategy for the treatment of ischemia-reperfusion injury.Frontiers in cell and developmental biology · 2024Review
- Comprehensive review on the novel immunotherapy target: Leucine-rich repeat-containing 8A/volume-regulated anion channel.International journal of biological sciences · 2024Review
- Physiological roles of chloride ions in bodily and cellular functions.The journal of physiological sciences : JPS · 2023Review
- The Key Role of Astrocytes in Amyotrophic Lateral Sclerosis and Their Commitment to Glutamate Excitotoxicity.International journal of molecular sciences · 2023Review
- Syringin inhibits endogenous volume regulated anion channel currents of HEK293 cells in hypotonic circumstances.Pharmacology research & perspectives · 2023Article
- Cell death induction and protection by activation of ubiquitously expressed anion/cation channels. Part 3: the roles and properties of TRPM2 and TRPM7.Frontiers in cell and developmental biology · 2023Review
- Apoptotic volume decrease (AVD) in AFrontiers in physiology · 2023Article
- A SWELL time to develop the molecular pharmacology of the volume-regulated anion channel (VRAC).Channels (Austin, Tex.) · 2022Review
- Cancer as a Channelopathy-Appreciation of Complimentary Pathways Provides a Different Perspective for Developing Treatments.Cancers · 2022Review
- Molecular determinants underlying volume-regulated anion channel subunit-dependent oxidation sensitivity.The Journal of physiology · 2022Article
- Fas/CD95 Signaling Pathway in Damage-Associated Molecular Pattern (DAMP)-Sensing Receptors.Cells · 2022Review
- Astrocytic Glutamatergic Transmission and Its Implications in Neurodegenerative Disorders.Cells · 2022Review
- Zinc pyrithione activates the volume-regulated anion channel through an antioxidant-sensitive mechanism.American journal of physiology. Cell physiology · 2021Article
40 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptotic volume decrease is a pivotal event triggering a cell to undergo apoptosis and is induced by ionic effluxes resulting mainly from increased K(+) and Cl(-) conductances. Here, we demonstrate that in human epithelia HeLa cells both mitochondrion- and death receptor-mediated apoptosis inducers [staurosporine and Fas ligand or tumor necrosis factor (TNF)-alpha] rapidly activate Cl(-) currents that show properties phenotypical of volume-sensitive outwardly rectifying Cl(-) channel currents, including outward rectification, voltage-dependent inactivation gating at large positive potentials, inhibition by osmotic shrinkage, sensitivity to classic Cl(-) channel blockers, and dependence on cytosolic ATP. Staurosporine, but not Fas ligand or TNF-alpha, rapidly (within 30 min) increased the intracellular level of reactive oxygen species (ROS). A ROS scavenger and an NAD(P)H oxidase inhibitor blocked the current activation by staurosporine but not by Fas ligand or TNF-alpha. A ROS scavenger also inhibited apoptotic volume decrease, caspase-3 activation, and apoptotic cell death induced by staurosporine. Thus, it is concluded that an apoptosis-triggering anion conductance is carried by the volume-sensitive outwardly rectifying Cl(-) channel and that the channel activation on apoptotic stimulation with staurosporine, but not with Fas ligand or TNF-alpha, is mediated by ROS.
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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.