June 2021
Volume 62, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2021
Introduction of a novel animal model of subretinal fibrosis after choroidal neovascularization
Author Affiliations & Notes
  • Souska Zandi
    Ophthalmology, Inselspital Universitatsspital Bern, Bern, BE, Switzerland
  • Keijiro Ishikawa
    Ophthalmology, Kyushu Daigaku, Fukuoka, Fukuoka, Japan
  • Iori Wada
    Ophthalmology, Kyushu Daigaku, Fukuoka, Fukuoka, Japan
  • Shintaro Nakao
    Ophthalmology, National Hospital Organization, Kyushu Medical Center, Fukuoka, Kyushu, Japan
  • Laura Jahnke
    Ophthalmology, Inselspital Universitatsspital Bern, Bern, BE, Switzerland
  • Yuebing Li
    Ophthalmology, Inselspital Universitatsspital Bern, Bern, BE, Switzerland
  • Volker Enzmann
    Ophthalmology, Inselspital Universitatsspital Bern, Bern, BE, Switzerland
  • Martin Sebastian Zinkernagel
    Ophthalmology, Inselspital Universitatsspital Bern, Bern, BE, Switzerland
  • Footnotes
    Commercial Relationships   Souska Zandi, None; Keijiro Ishikawa, None; Iori Wada, None; Shintaro Nakao, None; Laura Jahnke, None; Yuebing Li, None; Volker Enzmann, None; Martin Zinkernagel, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science June 2021, Vol.62, 371. doi:
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      Souska Zandi, Keijiro Ishikawa, Iori Wada, Shintaro Nakao, Laura Jahnke, Yuebing Li, Volker Enzmann, Martin Sebastian Zinkernagel; Introduction of a novel animal model of subretinal fibrosis after choroidal neovascularization. Invest. Ophthalmol. Vis. Sci. 2021;62(8):371.

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

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Abstract

Purpose : Subretinal fibrosis can develop in the course of neovascular age-related macular degeneration (AMD) and can lead to further vision loss of AMD patients. Intravitreal anti-VEGF treatment can reduce the choroidal neovascularization (CNV), but not the subretinal fibrosis. Until now, there is no successful treatment nor established animal model for subretinal fibrosis. We aim to introduce a novel animal model of subretinal fibrosis that might facilitate the development of novel therapeutic strategies for the reduction or inhibition of subretinal fibrosis.

Methods : C57BL/6J mice underwent laser photocoagulation to induce CNV-related fibrosis. Mice were anesthetized, and pupils were dilated with 5% phenylephrine and 0.8% tropicamide. Using a 532-nm laser, a slit-lamp delivery system, and a cover glass as a contact lens, six spots (100 mW, 50 mm, 100 ms) were placed in each eye. Volume of CNV and fibrosis was quantified with optical coherence tomography (OCT) measurements and confocal microscopy of choroidal flat mounts stained with isolectin B (CNV) and type 1 collagen (fibrosis) every week after laser injury (d7, d14, d21, d28, d35, d42, d49, n=6 per timepoint). Additionally, we performed autofluorescence and fluorescence angiography at every timepoint to document CNV and fibrosis changes over time.

Results : From day 21 to day 49 after laser injury of mice eyes the CNV and leakage decreased and the subretinal fibrosis increased in OCT and fluorescence angiography. The expression of collagen 1 in lesions of choroidal flat mounts increased, whereas isolectin B decreased.

Conclusions : The current results indicate that the CNV-related fibrosis model can be used for screening of anti-fibrotic treatment of subretinal fibrosis in neovascular age-related macular degeneration.

This is a 2021 ARVO Annual Meeting abstract.

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