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• W582314625 abstract "Diabetic macular edema (DME) is a major cause of visual impairment. Although DME is generally believed to be a microvascular disease, dysfunction of the retinal pigment epithelium (RPE) can also contribute to its development. Advanced glycation end-products (AGE) are thought to be one of the key factors involved in the pathogenesis of diabetes in the eye, and we have previously demonstrated a rapid breakdown of RPE function following glycated-albumin (Glyc-alb, a common AGE mimetic) administration in monolayer cultures of fetal human RPE cells. Here we present new evidence that this response is attributed to apically oriented AGE receptors (RAGE). Moreover, time-lapse optical coherence tomography in Dutch-belted rabbits 48 h post intravitreal Glyc-alb injections demonstrated a significant decrease in RPE-mediated fluid resorption in vivo. In both the animal and tissue culture models, the response to Glyc-alb was blocked by the relatively selective RAGE antagonist, FPS-ZM1 and was also inhibited by ZM323881, a relatively selective vascular endothelial growth factor receptor 2 (VEGF-R2) antagonist. Our data establish that the Glyc-alb-induced breakdown of RPE function is mediated via specific RAGE and VEGF-R2 signaling both in vitro and in vivo. These results are consistent with the notion that the RPE is a key player in the pathogenesis of DME." @default.
• W582314625 created "2016-06-24" @default.
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• W582314625 date "2015-08-01" @default.
• W582314625 modified "2023-10-16" @default.
• W582314625 title "Receptor mediated disruption of retinal pigment epithelium function in acute glycated-albumin exposure" @default.
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• W582314625 doi "https://doi.org/10.1016/j.exer.2015.06.004" @default.
• W582314625 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4523492" @default.
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