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REVIEW
Year : 2022  |  Volume : 17  |  Issue : 6  |  Page : 1183-1189

Microglial voltage-gated proton channel Hv1 in spinal cord injury


1 Department of Neurology, Mayo Clinic, Rochester, MN, USA
2 Department of Neurosurgery, Rutgers Robert Wood Johnson Medical School, Piscataway, NJ, USA
3 Department of Neurology, Mayo Clinic, Rochester; Department of Neuroscience, Mayo Clinic, Jacksonville; Department of Immunology, Mayo Clinic, Rochester, MN, USA

Correspondence Address:
Long-Jun Wu
Department of Neurology, Mayo Clinic, Rochester; Department of Neuroscience, Mayo Clinic, Jacksonville; Department of Immunology, Mayo Clinic, Rochester, MN
USA
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Source of Support: The work was supported by the National Institutes of Health (Nos. R01NS110949, R01NS088627, R01NS112144, R01NS110825, R21AG064159) to LJW, Conflict of Interest: None


DOI: 10.4103/1673-5374.327325

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After spinal cord injury, microglia as the first responders to the lesion display both beneficial and detrimental characteristics. Activated microglia phagocyte and eliminate cell debris, release cytokines to recruit peripheral immune cells to the injury site. Excessively activated microglia can aggravate the secondary damage by producing extravagant reactive oxygen species and pro-inflammatory cytokines. Recent studies demonstrated that the voltage-gated proton channel Hv1 is selectively expressed in microglia and regulates microglial activation upon injury. In mouse models of spinal cord injury, Hv1 deficiency ameliorates microglia activation, resulting in alleviated production of reactive oxygen species and pro-inflammatory cytokines. The reduced secondary damage subsequently decreases neuronal loss and correlates with improved locomotor recovery. This review provides a brief historical perspective of advances in investigating voltage-gated proton channel Hv1 and home in on microglial Hv1. We discuss recent studies on the roles of Hv1 activation in pathophysiological activities of microglia, such as production of NOX-dependent reactive oxygen species, microglia polarization, and tissue acidosis, particularly in the context of spinal cord injury. Further, we highlight the rationale for targeting Hv1 for the treatment of spinal cord injury and related disorders.


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