June 2020
Volume 61, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2020
Role of monocyte depletion on corneal neovascularization after herpes simplex virus type 1 (HSV-1) infection in Mouse Fas-Induced Apoptosis (MaFIA) model.
Author Affiliations & Notes
  • Adrian Filiberti
    Ophtalmology, Oklahoma University, Oklahoma City, Oklahoma, United States
  • Gmyrek Grzegorz
    Ophtalmology, Oklahoma University, Oklahoma City, Oklahoma, United States
  • Micaela Montgomery
    Ophtalmology, Oklahoma University, Oklahoma City, Oklahoma, United States
  • Renee Sallack
    Ophtalmology, Oklahoma University, Oklahoma City, Oklahoma, United States
  • Daniel J Carr
    Ophtalmology, Oklahoma University, Oklahoma City, Oklahoma, United States
  • Footnotes
    Commercial Relationships   Adrian Filiberti, None; Gmyrek Grzegorz, None; Micaela Montgomery, None; Renee Sallack, None; Daniel Carr, None
  • Footnotes
    Support  NIH R01 EY021238
Investigative Ophthalmology & Visual Science June 2020, Vol.61, 4071. doi:
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      Adrian Filiberti, Gmyrek Grzegorz, Micaela Montgomery, Renee Sallack, Daniel J Carr; Role of monocyte depletion on corneal neovascularization after herpes simplex virus type 1 (HSV-1) infection in Mouse Fas-Induced Apoptosis (MaFIA) model.. Invest. Ophthalmol. Vis. Sci. 2020;61(7):4071.

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

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Abstract

Purpose : HSV-1-induced corneal neovascularization (NV, blood and lymphatic vessel genesis) is essential but not exclusively driven by the upregulation of the pro-angiogenic factor vascular endothelial growth factor-A. Experimental evidence shows that other angiogenic factors contribute to vessel progression and maintenance. In addition, previous studies suggest macrophages also contribute to the NV process in other ocular inflammatory models. This study investigated the role of macrophages and angiogenic factors directly involved in HSV-1 induced-corneal NV.

Methods : Macrophages Fas-Induced Apoptosis (MaFIA) mice were infected with 500 plaque-forming units of HSV-1 in the cornea following scarification. From day 10 to 14 post-infection (pi), mice were treated with 40 µg/day of the B/B homodimerizer AP20187 (to deplete macrophages) or vehicle intraperitoneally. Corneas were harvested at 14 days pi and processed for immunohistochemistry to quantify corneal NV. The corneal content of pro- and anti-angiogenic factors was identified by antibody array (Proteome Profile). Protein candidates were quantified by magnetic luminex assays. Macrophage depletion was confirmed by flow cytometry.

Results : As previously described, HSV-1 elicited blood and lymphatic vessel growth into the central cornea in mice. In the absence of macrophages, vessel genesis was muted. These results correlated with a loss in fibroblast growth factor (FGF-2) and an increase in osteopontin (OPN) protein expression in the cornea.

Conclusions : Our data suggest that macrophage depletion results in a significant reduction in HSV-1-induced corneal NV. This effect correlates with the downregulation of FGF-2 and an increase in OPN expression. This result confirms our previous observation and could explain the reduction in NV after macrophage depletion in this model as FGF-2 is a central pro-angiogenic factor.

This is a 2020 ARVO Annual Meeting abstract.

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