June 2022
Volume 63, Issue 7
Open Access
ARVO Annual Meeting Abstract  |   June 2022
CCR2+ monocytes critically contribute to subretinal fibrosis at the chronic stage of the disease.
Author Affiliations & Notes
  • Manon SZCZEPAN
    Queen's University Belfast School of Medicine Dentistry and Biomedical Sciences, Belfast, Belfast, United Kingdom
  • Maria Llorian-Salvador
    Queen's University Belfast School of Medicine Dentistry and Biomedical Sciences, Belfast, Belfast, United Kingdom
  • Matthias Mack
    Department of Internal Medicine II – Nephrology, Universitatsklinikum Regensburg Klinik und Poliklinik Innere Medizin II, Regensburg, Bayern, Germany
  • Mei Chen
    Queen's University Belfast School of Medicine Dentistry and Biomedical Sciences, Belfast, Belfast, United Kingdom
  • Heping Xu
    Queen's University Belfast School of Medicine Dentistry and Biomedical Sciences, Belfast, Belfast, United Kingdom
  • Footnotes
    Commercial Relationships   Manon SZCZEPAN None; Maria Llorian-Salvador None; Matthias Mack None; Mei Chen None; Heping Xu None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science June 2022, Vol.63, 25. doi:
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      Manon SZCZEPAN, Maria Llorian-Salvador, Matthias Mack, Mei Chen, Heping Xu; CCR2+ monocytes critically contribute to subretinal fibrosis at the chronic stage of the disease.. Invest. Ophthalmol. Vis. Sci. 2022;63(7):25.

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

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Abstract

Purpose : Subretinal macular fibrosis occurs in up to 50% of neovascular age-related macular degeneration (nAMD) eyes and is a major cause of anti-VEGF resistance in nAMD. Currently, there are no medications to prevent or treat macular fibrosis secondary to nAMD. The aim of this study was to investigate the role of CC-chemokine receptor 2 (CCR2) expressing monocytes in the development of the fibrovascular phenotype of nAMD.

Methods : Subretinal fibrosis was induced in C57BL/6J mice using the two-stage laser-induced protocol previously described by Little et al (2020). The dynamics of the fibrotic lesion and infiltrating macrophages were assessed by immunofluorescence staining of collagen-1, F4/80 and CCR2, respectively at days 0, 1, 3, 6 and 10 post-second laser. Circulating CCR2+ monocytes were depleted using the CCR2 depleting antibody, MC-21, from day 1 to day 5 (acute stage depletion) or from day 5 to day 10 (chronic stage depletion). The level of depletion was confirmed by flow cytometry. Vascular and fibrotic components of the fibrovascular membrane were examined at day 10 post-second laser by immunofluorescence staining of isolectin B4 and collagen-1, respectively.

Results : The fibrotic lesion size reaches its peak 3 days after the second laser. CCR2+F4/80+ macrophages were detected in and around the fibrotic lesion and their number increased from day 3 to 10 post-second laser. Depletion of CCR2+ monocytes at the acute stage of disease did not affect the size of subretinal fibrosis. However, depletion of CCR2+ monocytes at the chronic stage of the disease significantly reduced the vascular and fibrotic components of the fibrovascular membrane.

Conclusions : Our results suggest that CCR2+ monocytes play a critical role in the development of the fibrovascular phenotype of nAMD during the chronic stage of inflammation. The underlying mechanism of CCR2+monocytes in promoting subretinal fibrosis warrants further investigation.

This abstract was presented at the 2022 ARVO Annual Meeting, held in Denver, CO, May 1-4, 2022, and virtually.

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