Neuroinflammation and gliosis in the injured and contralateral retinas after unilateral optic nerve crush

Exp Eye Res. 2023 Oct:235:109627. doi: 10.1016/j.exer.2023.109627. Epub 2023 Aug 22.

Abstract

The main purpose of this study is to analyze the effects of unilateral optic nerve crush in the gene expression of pro- and anti-inflammatory mediators, and gliosis markers in injured and contralateral retinas. Retinas from intact, unilaterally optic nerve injured or sham-operated C57BL/6J mice were analyzed 1, 3, 9 and 30 days after the surgery (n = 5/group and time point) and the relative expression of TGF-β1, IL-1β, TNF-α, Iba1, AQP4, GFAP, MHCII, and TSPO was analyzed in injured and contralateral using qPCR. The results indicated that compared with intact retinas, sham-operated animals showed an early (day 1) upregulation of IL-1β, TNF-α and TSPO and a late (day 30) upregulation of TNF-α. In sham-contralateral retinas, TNF-α and TSPO mRNA expression were upregulated and day 30 while GFAP, Iba1, AQP4 and MHCII downregulated at day 9. Compared with sham-operated animals, in retinas affected by optic nerve crush GFAP and TSPO upregulated at day 1 and TNF-α, Iba1, AQP4 and MHCII at day 3. In the crushed-contralateral retinas, TGF-β1, TNF-α, Iba1 and MHCII were upregulated at day 1. TSPO was upregulated up to day 30 whereas TGF-β1 and Iba1 downregulated after day 9. In conclusion, both sham surgery and optic nerve crush changed the profile of inflammatory and gliosis markers in the injured and contralateral retinas, changes that were more pronounced for optic nerve crush when compared to sham.

Keywords: Bilateral response; Cytokines; Gliosis; Inflammation; Microglial cells; Optic nerve crush; Retina.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Gliosis / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Nerve Crush / methods
  • Neuroinflammatory Diseases
  • Optic Nerve / metabolism
  • Optic Nerve Injuries* / genetics
  • Optic Nerve Injuries* / metabolism
  • Retina / metabolism
  • Retinal Ganglion Cells / metabolism
  • Transforming Growth Factor beta1* / pharmacology
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Transforming Growth Factor beta1
  • Tumor Necrosis Factor-alpha