ArticleBrain, behavior, and immunity2021
The voltage-gated proton channel Hv1 plays a detrimental role in contusion spinal cord injury via extracellular acidosis-mediated neuroinflammation.
Article in Brain, behavior, and immunity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 68 citations in OpenAlex.
- Phagocytosis and neuroinflammation: orchestrating central nervous system homeostasis, repair, and the resolution of inflammation.Trends in neurosciences · 2026Review
- Spinal motor neuron degeneration after brachial plexus avulsion: mechanisms and therapeutic targets.Frontiers in neuroscience · 2026Review
- Neuroprotection and Axonal Regeneration via ECM-Mimetic Nanofibers Incorporating Metal-Phenolic Network Nanoparticles Toward Spinal Cord Injury Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Kaempferide Promotes Neuroprotection and Functional Recovery After Spinal Cord Injury and is Associated with Differential Regulation of ARG1, CA4, CYP1B1, and OAT.Neuropsychiatric disease and treatment · 2026Article
- Machine learning-driven prediction of in-hospital cardiac arrest among critically ill patients with traumatic spinal cord injury: a multicenter cohort study.Frontiers in cardiovascular medicine · 2026Article
- Hv1 inhibition rescues AD pathology by restoring microglial mitochondrial function and enhancing mitochondrial transfer.Experimental & molecular medicine · 2025Article
- C6 peptide blockade of Hv1 channels inhibits neutrophil migration into the lungs to suppress Pseudomonas aeruginosa-induced acute lung injury.Respiratory research · 2025Article
- Forced polarisation of microglia by IL-13 is modified by inflammatory and microenvironmental context.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Hv1 channel in immune cells and pharmacology.Pharmacological research · 2025Review
- Validation of HvFrontiers in cellular neuroscience · 2025Article
- Acid-sensing ion channel-1 contributes to the failure of myelin sheath regeneration following spinal cord injury by transcellular delivery of PGE2.Cellular & molecular biology letters · 2024Article
- Article
- Spinal cord injury disrupts plasma extracellular vesicles cargoes leading to neuroinflammation in the brain and neurological dysfunction in aged male mice.Brain, behavior, and immunity · 2024Article
- Repair spinal cord injury with a versatile anti-oxidant and neural regenerative nanoplatform.Journal of nanobiotechnology · 2024Article
- The Emerging Role of Microglial Hv1 as a Target for Immunomodulation in Myelin Repair.Aging and disease · 2024Review
- Ablation of the integrin CD11b mac-1 limits deleterious responses to traumatic spinal cord injury and improves functional recovery in mice.Research square · 2024Article
- Tuning neural circuits and behaviors by microglia in the adult brain.Trends in neurosciences · 2024Review
- Role of S100 and YKL40 on Intraventricular Cerebral Hemorrhages in the Preterm Infant and the Neuroprotective Role of miR-138- siRNAs-HIF-1a and miR-21-siRNAs-HVCN1 in Neonatal Mice with Nerve Injury.Current medicinal chemistry · 2024Article
- Inhibition of the HFrontiers in immunology · 2024Article
- Mechanically-primed voltage-gated proton channels from angiosperm plants.Nature communications · 2023Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Tissue acidosis is an important secondary injury process in the pathophysiology of traumatic spinal cord injury (SCI). To date, no studies have examined the role of proton extrusion as mechanism of pathological acidosis in SCI. In the present study, we hypothesized that the phagocyte-specific proton channel Hv1 mediates hydrogen proton extrusion after SCI, contributing to increased extracellular acidosis and poor long-term outcomes. Using a contusion model of SCI in adult female mice, we demonstrated that tissue pH levels are markedly lower during the first week after SCI. Acidosis was most evident at the injury site, but also extended into proximal regions of the cervical and lumbar cord. Tissue reactive oxygen species (ROS) levels and expression of Hv1 were significantly increased during the week of injury. Hv1 was exclusively expressed in microglia within the CNS, suggesting that microglia contribute to ROS production and proton extrusion during respiratory burst. Depletion of Hv1 significantly attenuated tissue acidosis, NADPH oxidase 2 (NOX2) expression, and ROS production at 3 d post-injury. Nanostring analysis revealed decreased gene expression of neuroinflammatory and cytokine signaling markers in Hv1 knockout (KO) mice. Furthermore, Hv1 deficiency reduced microglia proliferation, leukocyte infiltration, and phagocytic oxidative burst detected by flow cytometry. Importantly, Hv1 KO mice exhibited significantly improved locomotor function and reduced histopathology. Overall, these data suggest an important role for Hv1 in regulating tissue acidosis, NOX2-mediated ROS production, and functional outcome following SCI. Thus, the Hv1 proton channel represents a potential target that may lead to novel therapeutic strategies for SCI.
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