June 2023
Volume 64, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2023
Interleukin (IL)-17A enhances retinal vascular angiogenesis and neovascularization in oxygen induced retinopathy
Author Affiliations & Notes
  • Brooklyn E Taylor
    Ophthalmology, Case Western Reserve University, Cleveland, Ohio, United States
  • Chieh Lee
    Ophthalmology, Case Western Reserve University, Cleveland, Ohio, United States
  • Thomas Eugene Zapadka
    Ophthalmology, Case Western Reserve University, Cleveland, Ohio, United States
  • Scott J Howell
    Ophthalmology, Case Western Reserve University, Cleveland, Ohio, United States
    Research, VA Northeast Ohio Healthcare System, Cleveland, Ohio, United States
  • Patricia R Taylor
    Ophthalmology, Case Western Reserve University, Cleveland, Ohio, United States
    Research, VA Northeast Ohio Healthcare System, Cleveland, Ohio, United States
  • Footnotes
    Commercial Relationships   Brooklyn Taylor None; Chieh Lee None; Thomas Zapadka None; Scott Howell None; Patricia Taylor None
  • Footnotes
    Support  NIH R01 EY030487, NIH U01 EY034693, VA Merit CX002204
Investigative Ophthalmology & Visual Science June 2023, Vol.64, 2050. doi:
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    • Get Citation

      Brooklyn E Taylor, Chieh Lee, Thomas Eugene Zapadka, Scott J Howell, Patricia R Taylor; Interleukin (IL)-17A enhances retinal vascular angiogenesis and neovascularization in oxygen induced retinopathy. Invest. Ophthalmol. Vis. Sci. 2023;64(8):2050.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : Interleukin (IL)-17A has been previously reported to play a role in age-related macular degeneration, glaucoma, and diabetic retinopathy. Although retinal neovascularization can lead to vision loss in all of these ocular diseases, the role of IL-17A in retinal vascular angiogenesis and neovascularization is unclear. In other diseases, IL-17A enhances angiogenesis. Hence, we hypothesized that IL-17A enhances retinal vascular angiogenesis and neovascularization.

Methods : Human Muller glia and retinal endothelial cells (100,000 cells/well) were unstimulated or stimulated with 20ng/ml of recombinant IL-17A for 16h, and levels of VEGFA was quantified in the supernatants (n=6/group) by ELISA. Further, angiogenesis was examined in 10,000 unstimulated or IL-17A stimulated (20ng/ml) human retinal endothelial cells (hREC) using WimTube software. Additionally, cellular proliferation was examined in unstimulated, IL-17A, VEGFA, or IL-17A+VEGFA (20ng/ml of each) stimulated hREC by BrdU analysis. Finally, retinal neovascularization was examined in vivo using the oxygen induced retinopathy model in wild-type C57BL/6 and IL17A-/- mice (n=5/group). Briefly, 7-day-old mice were placed into a 75% oxygen chamber for 5 days, then placed into normal room air for 5 days, prior to analysis of 17-day old mice. Retinas were collected from euthanized mice and neovascularization of isolectin stained whole mounts was quantified.

Results : When human Muller glia and retinal endothelial cells were incubated with 20ng/ml of recombinant IL-17A, VEGFA production was induced. This same concentration of recombinant IL-17A also induced retinal endothelial cell angiogenesis per WimTube and BrdU analysis. Additionally, VEGF-induced proliferation in human retinal endothelial cells was significantly increased (p<0.05) when IL-17A was added. Finally, there was a significant decrease in neovascularization of IL17A-/- than wild-type C57BL/6 mice when retinal vascular proliferation was induced using the oxygen induced retinopathy model.

Conclusions : These results support our hypothesis that IL-17A enhances retinal vascular angiogenesis and neovascularization. Further in vivo studies of ocular disease specific neovascularization will be needed to define the role of IL-17A in neovascular glaucoma and proliferative diabetic retinopathy.

This abstract was presented at the 2023 ARVO Annual Meeting, held in New Orleans, LA, April 23-27, 2023.

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