Cytotoxic effect of interleukin-8 in retinal ganglion cells and its possible mechanisms

Jing-Jing Wang1, Walana Williams1, Bing Wang1

  • 1Department of Immunology, Dalian Medical University, Dalian 116044, Liaoning Province, China.

Abstract

Insights

Interleukin-8 (IL-8) inhibits neural retinal ganglion cell viability and promotes apoptosis. The specific receptor antagonist G31P partially reverses these detrimental effects, offering a potential therapeutic avenue.

Area of Science:

  • Ophthalmology
  • Neuroscience
  • Immunology

Background:

  • Neural retinal ganglion cells (RGCs) are crucial for vision.
  • Interleukin-8 (IL-8) is a pro-inflammatory cytokine implicated in various cellular processes.

Purpose of the Study:

  • To determine the impact of IL-8 on RGC viability and apoptosis.
  • To evaluate the potential protective effect of G31P, an IL-8 receptor antagonist, against IL-8-induced RGC damage.

Main Methods:

  • RGC-5 cells were treated with IL-8 and/or G31P.
  • Cell viability was assessed using CCK-8 assays.
  • Apoptosis was quantified via nuclear morphology and flow cytometry.
  • Gene and protein expression of apoptosis-related markers (Bcl-2, Bax, caspase-3) were analyzed using RT-qPCR and Western blot.

Main Results:

  • IL-8 significantly reduced RGC-5 cell viability in a dose-dependent manner.
  • IL-8 treatment increased the apoptotic rate of RGCs.
  • IL-8 upregulated pro-apoptotic Bax and caspase-3 while downregulating anti-apoptotic Bcl-2 at both mRNA and protein levels.
  • G31P pre-treatment partially mitigated the effects of IL-8 on RGC viability and apoptosis.

Conclusions:

  • IL-8 exerts anti-proliferative effects on RGCs by inducing apoptosis.
  • The observed apoptosis is mediated by the modulation of Bcl-2, Bax, and caspase-3 expression.
  • G31P demonstrates a protective effect, ameliorating IL-8-induced RGC apoptosis.

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