Blue-violet light decreases VEGFa production in an in vitro model of AMD.
Blue light is an identified risk factor for age-related macular degeneration (AMD). The production of vascular endothelial growth factor (VEGF), leading to neovascularization, is a major complication of the wet form of this disease. We investigated how blue light affects VEGF expression and secretio...
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doaj-8c5588b18e5c4e78bc7d754fb6a2a7a12021-03-03T21:15:38ZengPublic Library of Science (PLoS)PLoS ONE1932-62032019-01-011410e022383910.1371/journal.pone.0223839Blue-violet light decreases VEGFa production in an in vitro model of AMD.Mélanie MariePauline GondouinDelphine PaganCoralie BarrauThierry VilletteJosé SahelSerge PicaudBlue light is an identified risk factor for age-related macular degeneration (AMD). The production of vascular endothelial growth factor (VEGF), leading to neovascularization, is a major complication of the wet form of this disease. We investigated how blue light affects VEGF expression and secretion using A2E-loaded retinal pigment epithelium (RPE) cells, a cell model of AMD. Incubation of RPE cells with A2E resulted in a significant increase in VEGF mRNA and, intracellular and secreted VEGF protein levels, but not mRNA levels of VEGFR1 or VEGFR2. Blue light exposure of A2E-loaded RPE cells resulted in a decrease in VEGF mRNA and protein levels, but an increase in VEGFR1 levels. The toxicity of 440 nm light on A2E-loaded RPE cells was enhanced by VEGF supplementation. Our results suggest that age-related A2E accumulation may result in VEGF synthesis and release. This synthesis of VEGF, which enhances blue light toxicity for the RPE cells, is itself suppressed by blue light. Anti-VEGF therapy may therefore improve RPE survival in AMD.https://doi.org/10.1371/journal.pone.0223839 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Mélanie Marie Pauline Gondouin Delphine Pagan Coralie Barrau Thierry Villette José Sahel Serge Picaud |
spellingShingle |
Mélanie Marie Pauline Gondouin Delphine Pagan Coralie Barrau Thierry Villette José Sahel Serge Picaud Blue-violet light decreases VEGFa production in an in vitro model of AMD. PLoS ONE |
author_facet |
Mélanie Marie Pauline Gondouin Delphine Pagan Coralie Barrau Thierry Villette José Sahel Serge Picaud |
author_sort |
Mélanie Marie |
title |
Blue-violet light decreases VEGFa production in an in vitro model of AMD. |
title_short |
Blue-violet light decreases VEGFa production in an in vitro model of AMD. |
title_full |
Blue-violet light decreases VEGFa production in an in vitro model of AMD. |
title_fullStr |
Blue-violet light decreases VEGFa production in an in vitro model of AMD. |
title_full_unstemmed |
Blue-violet light decreases VEGFa production in an in vitro model of AMD. |
title_sort |
blue-violet light decreases vegfa production in an in vitro model of amd. |
publisher |
Public Library of Science (PLoS) |
series |
PLoS ONE |
issn |
1932-6203 |
publishDate |
2019-01-01 |
description |
Blue light is an identified risk factor for age-related macular degeneration (AMD). The production of vascular endothelial growth factor (VEGF), leading to neovascularization, is a major complication of the wet form of this disease. We investigated how blue light affects VEGF expression and secretion using A2E-loaded retinal pigment epithelium (RPE) cells, a cell model of AMD. Incubation of RPE cells with A2E resulted in a significant increase in VEGF mRNA and, intracellular and secreted VEGF protein levels, but not mRNA levels of VEGFR1 or VEGFR2. Blue light exposure of A2E-loaded RPE cells resulted in a decrease in VEGF mRNA and protein levels, but an increase in VEGFR1 levels. The toxicity of 440 nm light on A2E-loaded RPE cells was enhanced by VEGF supplementation. Our results suggest that age-related A2E accumulation may result in VEGF synthesis and release. This synthesis of VEGF, which enhances blue light toxicity for the RPE cells, is itself suppressed by blue light. Anti-VEGF therapy may therefore improve RPE survival in AMD. |
url |
https://doi.org/10.1371/journal.pone.0223839 |
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