July 2019
Volume 60, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2019
Influence of adipose tissue on choroidal neovascularization
Author Affiliations & Notes
  • Roberto Diaz Marin
    Biochemistry, Montreal University, Montreal, Quebec, Canada
    Centre de Recherche HMR, Montreal, Quebec, Canada
  • Sergio Crespo-Garcia
    Biochemistry, Montreal University, Montreal, Quebec, Canada
    Centre de Recherche HMR, Montreal, Quebec, Canada
  • Frederik Fournier
    Biochemistry, Montreal University, Montreal, Quebec, Canada
    Centre de Recherche HMR, Montreal, Quebec, Canada
  • Vincent De Guire
    Centre de Recherche HMR, Montreal, Quebec, Canada
  • Przemyslaw Sapieha
    Biochemistry, Montreal University, Montreal, Quebec, Canada
    Ophthalmology, McGill University, Montreal, Quebec, Canada
  • Footnotes
    Commercial Relationships   Roberto Diaz Marin, None; Sergio Crespo-Garcia, None; Frederik Fournier, None; Vincent De Guire, None; Przemyslaw Sapieha, None
  • Footnotes
    Support  Foundation Fighting Blindness
Investigative Ophthalmology & Visual Science July 2019, Vol.60, 1262. doi:https://doi.org/
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    • Get Citation

      Roberto Diaz Marin, Sergio Crespo-Garcia, Frederik Fournier, Vincent De Guire, Przemyslaw Sapieha; Influence of adipose tissue on choroidal neovascularization. Invest. Ophthalmol. Vis. Sci. 2019;60(9):1262. doi: https://doi.org/.

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

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Abstract

Purpose : Obesity leads to deregulation of adipose tissue (AT) homeostasis. While obesity is an important risk factor for age-related macular degeneration (AMD), how the AT influences AMD is poorly understood. AT browning is the biochemical conversion of white adipocytes into brite adipocytes, and this process is reduced during obesity and ageing. Browning has been shown to be regulated by sympathetic nervous system (SNS) catecholamines. Based on previous research that showed a relation of choroidal neovascularization (CNV) with the SNS, our goal was to assess the impact of loss of AT browning on the pathogenesis of neovascular AMD in a mouse model.

Methods : Laser induced CNV was induced in male C57BL/6J mice (4 impacts/eye, 400mV, 50µm diameter, 0.05sec duration); none lasered, but handled animals served as controls. AT browning and inflammation was evaluated by RT-qPCR and Western blot in white (WAT), beige (BgAT) and brown (BAT) adipose tissues during the course of CNV (3, 7 and 14 days after laser injury). Plasma levels of catecholamines were measured at 3 and 7 days post-injury.

Results : In the early phase of CNV (3 and 7 days after laser), only BgAT showed an increase in browning protein markers (UCP1 & PGC1α), whereas WAT and BAT were unaffected. In the late phase of CNV (14 days after laser), UCP1 protein levels were significantly downregulated in BgAT. Gene expression analysis confirmed these results and, interestingly, showed that inflammatory markers (Il6, Tnfα and Il1β) were upregulated in BgAT in the late phase. WAT showed an increase in gene expression of browning markers in the late CNV phase. Systemic catecholamines were more abundant in the early CNV phase.

Conclusions : Our data demonstrates that laser CNV can trigger expression of browning markers and induce inflammation in AT. These findings contribute to our fundamental understanding of the role of AT in AMD.

This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.

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