Mechanistic insight into the suppression of microglial ROS production by voltage-gated proton channels (VSOP/Hv1)

Channels (Austin). 2018 Jan 1;12(1):1-8. doi: 10.1080/19336950.2017.1385684. Epub 2017 Nov 17.


Voltage-gated proton channels (VSOP/Hv1) reportedly promote reactive oxygen species (ROS) production in several immune cell types. However, we recently reported that primary microglia from VSOP/Hv1-deficient mice show higher ROS production than those from WT mice. Microglia may show a distinct activation status between WT and VSOP/Hv1-deficient cells, leading to a distinct level of ROS production between them. This is unlikely, however, because ROS production in VSOP/Hv1-deficient microglia remained higher than in WT microglia when the cells were exposed to LPS. Further, this increase in ROS production in VSOP/Hv1-deficient cells was not observed in macrophages, which suggests microglia have a unique mechanism of VSOP/Hv1-dependent ROS regulation. The mechanism underlying this unconventional ROS regulation by VSOP/Hv1 in microglia is discussed.

Keywords: ROS; VSOP/Hv1; microglia; microglial activation; voltage-gated proton channel.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Ion Channels / deficiency
  • Ion Channels / metabolism*
  • Mice
  • Mice, Knockout
  • Microglia / metabolism*
  • Reactive Oxygen Species / antagonists & inhibitors*
  • Reactive Oxygen Species / metabolism


  • Hv1 proton channel, mouse
  • Ion Channels
  • Reactive Oxygen Species