Microglial voltage-gated proton channel Hv1 in spinal cord injury

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 agg...

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Autores principales:	Jiaying Zheng, Madhuvika Murugan, Lingxiao Wang, Long-Jun Wu
Formato:	article
Lenguaje:	EN
Publicado:	Wolters Kluwer Medknow Publications 2022
Materias:	hv1 proton channel; ion channels; microglia; nadph oxidase; ph regulation; reactive oxygen species; spinal cord injury Neurology. Diseases of the nervous system RC346-429
Acceso en línea:	https://doaj.org/article/a8a094702ac24906b834500d5d908440
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spelling	oai:doaj.org-article:a8a094702ac24906b834500d5d9084402021-11-19T12:16:44ZMicroglial voltage-gated proton channel Hv1 in spinal cord injury1673-537410.4103/1673-5374.327325https://doaj.org/article/a8a094702ac24906b834500d5d9084402022-01-01T00:00:00Zhttp://www.nrronline.org/article.asp?issn=1673-5374;year=2022;volume=17;issue=6;spage=1183;epage=1189;aulast=Zhenghttps://doaj.org/toc/1673-5374After 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.Jiaying ZhengMadhuvika MuruganLingxiao WangLong-Jun WuWolters Kluwer Medknow Publicationsarticlehv1 proton channel; ion channels; microglia; nadph oxidase; ph regulation; reactive oxygen species; spinal cord injuryNeurology. Diseases of the nervous systemRC346-429ENNeural Regeneration Research, Vol 17, Iss 6, Pp 1183-1189 (2022)
institution	DOAJ
collection	DOAJ
language	EN
topic	hv1 proton channel; ion channels; microglia; nadph oxidase; ph regulation; reactive oxygen species; spinal cord injury Neurology. Diseases of the nervous system RC346-429
spellingShingle	hv1 proton channel; ion channels; microglia; nadph oxidase; ph regulation; reactive oxygen species; spinal cord injury Neurology. Diseases of the nervous system RC346-429 Jiaying Zheng Madhuvika Murugan Lingxiao Wang Long-Jun Wu Microglial voltage-gated proton channel Hv1 in spinal cord injury
description	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.
format	article
author	Jiaying Zheng Madhuvika Murugan Lingxiao Wang Long-Jun Wu
author_facet	Jiaying Zheng Madhuvika Murugan Lingxiao Wang Long-Jun Wu
author_sort	Jiaying Zheng
title	Microglial voltage-gated proton channel Hv1 in spinal cord injury
title_short	Microglial voltage-gated proton channel Hv1 in spinal cord injury
title_full	Microglial voltage-gated proton channel Hv1 in spinal cord injury
title_fullStr	Microglial voltage-gated proton channel Hv1 in spinal cord injury
title_full_unstemmed	Microglial voltage-gated proton channel Hv1 in spinal cord injury
title_sort	microglial voltage-gated proton channel hv1 in spinal cord injury
publisher	Wolters Kluwer Medknow Publications
publishDate	2022
url	https://doaj.org/article/a8a094702ac24906b834500d5d908440
work_keys_str_mv	AT jiayingzheng microglialvoltagegatedprotonchannelhv1inspinalcordinjury AT madhuvikamurugan microglialvoltagegatedprotonchannelhv1inspinalcordinjury AT lingxiaowang microglialvoltagegatedprotonchannelhv1inspinalcordinjury AT longjunwu microglialvoltagegatedprotonchannelhv1inspinalcordinjury
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Microglial voltage-gated proton channel Hv1 in spinal cord injury

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