2014
DOI: 10.1167/iovs.14-14217
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Modulation of VEGF-Induced Retinal Vascular Permeability by Peroxisome Proliferator-Activated Receptor- / 

Abstract: These data suggest a protective effect for PPARβ/δ antagonism against VEGF-induced vascular permeability, possibly through reduced VEGFR expression. Therefore, antagonism/reverse agonism of PPARβ/δ siRNA may represent a novel therapeutic methodology against retinal hyperpermeability and is worthy of future investigation.

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Cited by 38 publications
(39 citation statements)
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“…Claudin-1 is present in the tight junctions between endothelial cells of retinal vessels [26,27]. In addition, Claudin-1 gene expression is suppressed following VEGF treatment [28]. Our findings showed that hVEGF treatment decreased Claudin-1 levels while FGF21 co-treatment preserved Claudin-1 levels.…”
Section: Discussionmentioning
confidence: 51%
“…Claudin-1 is present in the tight junctions between endothelial cells of retinal vessels [26,27]. In addition, Claudin-1 gene expression is suppressed following VEGF treatment [28]. Our findings showed that hVEGF treatment decreased Claudin-1 levels while FGF21 co-treatment preserved Claudin-1 levels.…”
Section: Discussionmentioning
confidence: 51%
“…Modeling retinal neovascularization, it was shown that pharmacological antagonism of PPARβ/δ significantly decreased serum-induced retinal endothelial cell proliferation and tube formation in a dose-dependent manner, and in vivo decreased retinal neovascularization in young rats. Another study from the same group showed that pharmacological antagonism of PPARβ/δ stabilized tight junctions in retinal microvascular endothelial cells treated with VEGF, and reduced VEGFR1/2 expression, suggesting a role in retinal vascular permeability [ 52 ]. The present study examined the effect of ligand activation and pharmacological antagonism of PPARβ/δ on choroidal neovascularization, in which the highly fenestrated choriocapillaris; vasculature supporting the outer retina; grow through Bruch's membrane under the RPE, in vivo , using a laser-induced CNV model.…”
Section: Discussionmentioning
confidence: 99%
“…Each well was transfected, as previously described81, with 200 ng NFkB-responsive luciferase constructs from the Cignal NFkB Reporter Assay (Qiagen). Cells were treated with vehicle or TNFα (1 ng/ml) in the presence or absence of 11,12-EET (0.5 μM) or 19,20-EDP (0.5 μM) with AUDA (10 μ M) for 24 hours after initiating transfection.…”
Section: Methodsmentioning
confidence: 99%