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 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.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2022 |
|---|---|
| Erschienen: |
2022 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:17 |
|---|---|
| Enthalten in: |
Neural regeneration research - 17(2022), 6 vom: 13. Juni, Seite 1183-1189 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Zheng, Jiaying [VerfasserIn] |
|---|
| Links: |
|---|
| Themen: |
Hv1 proton channel |
|---|
| Anmerkungen: |
Date Revised 08.11.2023 published: Print Citation Status PubMed-not-MEDLINE |
|---|
| doi: |
10.4103/1673-5374.327325 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM333202872 |
|---|
| LEADER | 01000naa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM333202872 | ||
| 003 | DE-627 | ||
| 005 | 20231225221152.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 231225s2022 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.4103/1673-5374.327325 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1110.xml |
| 035 | |a (DE-627)NLM333202872 | ||
| 035 | |a (NLM)34782552 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Zheng, Jiaying |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Microglial voltage-gated proton channel Hv1 in spinal cord injury |
| 264 | 1 | |c 2022 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Revised 08.11.2023 | ||
| 500 | |a published: Print | ||
| 500 | |a Citation Status PubMed-not-MEDLINE | ||
| 520 | |a 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 | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Review | |
| 650 | 4 | |a Hv1 proton channel | |
| 650 | 4 | |a NADPH oxidase | |
| 650 | 4 | |a ion channels | |
| 650 | 4 | |a microglia | |
| 650 | 4 | |a pH regulation | |
| 650 | 4 | |a reactive oxygen species | |
| 650 | 4 | |a spinal cord injury | |
| 700 | 1 | |a Murugan, Madhuvika |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Lingxiao |e verfasserin |4 aut | |
| 700 | 1 | |a Wu, Long-Jun |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Neural regeneration research |d 2012 |g 17(2022), 6 vom: 13. Juni, Seite 1183-1189 |w (DE-627)NLM234805757 |x 1673-5374 |7 nnns |
| 773 | 1 | 8 | |g volume:17 |g year:2022 |g number:6 |g day:13 |g month:06 |g pages:1183-1189 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.4103/1673-5374.327325 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 17 |j 2022 |e 6 |b 13 |c 06 |h 1183-1189 | ||