ArticleBMC immunology2013
Proton channel HVCN1 is required for effector functions of mouse eosinophils.
Article in BMC immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- Hv1 channel in immune cells and pharmacology.Pharmacological research · 2025Review
- Ion Channels in the Immune Response of Asthma.Journal of respiratory biology and translational medicine · 2024Article
- Role of the Voltage-Gated Proton Channel Hv1 in Nervous Systems.Neuroscience bulletin · 2023Review
- Voltage-Gated Proton Channels in the Tree of Life.Biomolecules · 2023Review
- Role of voltage-gated proton channel (Hv1) in cancer biology.Frontiers in pharmacology · 2023Review
- Microglial voltage-gated proton channel Hv1 in spinal cord injury.Neural regeneration research · 2022Review
- Semaphorin-3 Promotes Specific Immunotherapy Effects on Experimental Food Allergy.Journal of immunology research · 2022Article
- The voltage-gated proton channel Hv1 promotes microglia-astrocyte communication and neuropathic pain after peripheral nerve injury.Molecular brain · 2021Article
- Regulation of Neutrophil Functions by Hv1/VSOP Voltage-Gated Proton Channels.International journal of molecular sciences · 2021Review
- Thermodynamics and Mechanism of the Membrane Permeation of Hv1 Channel Blockers.The Journal of membrane biology · 2021Article
- Functions and Mechanisms of the Voltage-Gated Proton Channel Hv1 in Brain and Spinal Cord Injury.Frontiers in cellular neuroscience · 2021Review
- Zinc modulation of proton currents in a new voltage-gated proton channel suggests a mechanism of inhibition.The FEBS journal · 2020Article
- Insights on small molecule binding to the Hv1 proton channel from free energy calculations with molecular dynamics simulations.Scientific reports · 2020Article
- Voltage and pH sensing by the voltage-gated proton channel, HJournal of the Royal Society, Interface · 2018Review
- Mechanistic insight into the suppression of microglial ROS production by voltage-gated proton channels (VSOP/Hv1).Channels (Austin, Tex.) · 2018Article
- The intimate and controversial relationship between voltage-gated proton channels and the phagocyte NADPH oxidase.Immunological reviews · 2016Review
- Microglial Hv1 proton channel promotes cuprizone-induced demyelination through oxidative damage.Journal of neurochemistry · 2015Article
- Voltage-Gated Proton Channels as Novel Drug Targets: From NADPH Oxidase Regulation to Sperm Biology.Antioxidants & redox signaling · 2015Review
- The Voltage-Gated Proton Channel: A Riddle, Wrapped in a Mystery, inside an Enigma.Biochemistry · 2015Review
- Regulation of immune responses by proton channels.Immunology · 2014Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundProton currents are required for optimal respiratory burst in phagocytes. Recently, HVCN1 was identified as the molecule required for the voltage-gated proton channel activity associated with the respiratory burst in neutrophils. Although there are similarities between eosinophils and neutrophils regarding their mechanism for respiratory burst, the role of proton channels in eosinophil functions has not been fully understood.
resultsIn the present study, we first identified the expression of the proton channel HVCN1 in mouse eosinophils. Furthermore, using HVCN1-deficient eosinophils, we demonstrated important cell-specific effector functions for HVCN1. Similar to HVCN1-deficient neutrophils, HVCN1-deficient eosinophils produced significantly less reactive oxygen species (ROS) upon phorbol myristate acetate (PMA) stimulation compared with WT eosinophils. In contrast to HVCN1-deficient neutrophils, HVCN1-deficient eosinophils did not show impaired calcium mobilization or migration ability compared with wild-type (WT) cells. Uniquely, HVCN1-deficient eosinophils underwent significantly increased cell death induced by PMA stimulation compared with WT eosinophils. The increased cell death was dependent on NADPH oxidase activation, and correlated with the failure of HVCN1-deficient cells to maintain membrane polarization and intracellular pH in the physiological range upon activation.
conclusionsEosinophils require proton channel HVCN1 for optimal ROS generation and prevention of activation-induced cell death.
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Registered trials
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.