Redox regulation of soluble epoxide hydrolase does not affect pain behavior in mice

Neurosci Lett. 2020 Mar 16:721:134798. doi: 10.1016/j.neulet.2020.134798. Epub 2020 Jan 30.

Abstract

Signaling mediated by soluble epoxide hydrolase (sEH) has been reported to play an important role in pain processing. Previous studies revealed that sEH activity is inhibited by specific binding of electrophiles to a redox-sensitive thiol (Cys521) adjacent to the catalytic center of the hydrolase. Here, we investigated if this redox-dependent modification of sEH is involved in pain processing using "redox-dead" knockin-mice (sEH-KI), in which the redox-sensitive cysteine is replaced by serine. However, behavioral characterization of sEH-KI mice in various animal models revealed that acute nociceptive, inflammatory, neuropathic, and visceral pain processing is not altered in sEH-KI mice. Thus, our results suggest that redox-dependent modifications of sEH are not critically involved in endogenous pain signaling in mice.

Keywords: Mice; Pain; Redox signaling; Soluble epoxide hydrolase; sEH.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Epoxide Hydrolases / genetics
  • Epoxide Hydrolases / metabolism*
  • Mice
  • Mice, Transgenic
  • Oxidation-Reduction / drug effects
  • Pain / chemically induced
  • Pain / enzymology*
  • Pain Measurement / drug effects
  • Pain Measurement / methods*
  • Zymosan / toxicity

Substances

  • Zymosan
  • Epoxide Hydrolases
  • Ephx2 protein, mouse