ZNRF2 attenuates focal cerebral ischemia/reperfusion injury in rats by inhibiting mTORC1-mediated autophagy

Exp Neurol. 2021 Aug:342:113759. doi: 10.1016/j.expneurol.2021.113759. Epub 2021 May 13.

Abstract

Zinc and ring finger 2 (ZNRF2), an E3 ubiquitin ligase, plays a crucial role in many diseases. However, its role in cerebral ischemia/reperfusion injury (CIRI) still remains unknown. In this study, the function and molecular mechanism of ZNRF2 in CIRI in vivo and vitro was studied. ZNRF2 was found to be dramatically downregulated in CIRI. Overexpression of ZNRF2 could significantly reduce the neurological deficit, brain infarct volume and histopathological damage of cortex in middle cerebral artery occlusion/reperfusion. Concomitantly, overexpression of ZNRF2 increased the primary neuronal viability and decreased the neuronal apoptosis induced by oxygen-glucose deprivation and reoxygenation (OGD/R). Mechanistically, overexpression of ZNRF2 inhibited the over-induction of autophagy induced by OGD/R which was abolished by mTORC1 inhibitor rapamycin. It can be concluded that ZNRF2 plays a protective effect in CIRI and the underlying mechanism may be related to the inhibition of mTORC1-mediated autophagy.

Keywords: Autophagy; CIRI; OGD/R; Primary neurons; ZNRF2; mTOR.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Aged, 80 and over
  • Animals
  • Autophagy / physiology*
  • Brain Ischemia / metabolism
  • Brain Ischemia / prevention & control*
  • Female
  • Humans
  • Male
  • Mechanistic Target of Rapamycin Complex 1 / antagonists & inhibitors*
  • Mechanistic Target of Rapamycin Complex 1 / metabolism
  • Middle Aged
  • Rats
  • Rats, Sprague-Dawley
  • Reperfusion Injury / metabolism
  • Reperfusion Injury / prevention & control*
  • Ubiquitin-Protein Ligases / biosynthesis*
  • Ubiquitin-Protein Ligases / genetics

Substances

  • Ubiquitin-Protein Ligases
  • ZNRF2 protein, human
  • Mechanistic Target of Rapamycin Complex 1