RGD Reference Report - Suppression of Retinal Peroxisome Proliferator Activated Receptor-gamma in Experimental Diabetes and Oxygen-Induced Retinopathy: Role of NADPH Oxidase. - Rat Genome Database

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Suppression of Retinal Peroxisome Proliferator Activated Receptor-gamma in Experimental Diabetes and Oxygen-Induced Retinopathy: Role of NADPH Oxidase.

Authors: Tawfik, A  Sanders, T  Kahook, K  Akeel, S  El-Marakby, A  Al-Shabrawey, M 
Citation: Tawfik A, etal., Invest Ophthalmol Vis Sci. 2008 Sep 20.
RGD ID: 2301844
Pubmed: PMID:18806296   (View Abstract at PubMed)
DOI: DOI:10.1167/iovs.08-2005   (Journal Full-text)

Purpose: Recently we have shown that NADPH oxidase is positively correlated with increased leukocyte adhesion and vascular leakage in diabetes and neovascularization in oxygen-induced retinopathy (OIR). Peroxisome proliferator-activated receptor gamma (PPARgamma) agonists have been shown to prevent vascular inflammation and leakage in experimental model of diabetes. So, the goal of this study was to investigate whether there is a link between NADPH oxidase and PPARgamma that leads to vascular dysfunction in diabetic retina or OIR. Methods: Diabetes was induced with streptozotocin in wild type mice or NOX2 knockout mice. One group of wild type mice was treated with apocynin. Bovine retinal endothelial cells (BRECs) were treated with normal glucose (5 mM) or high glucose (25 mM) in the presence or absence of superoxide dismutase (SOD) or NADPH oxidase inhibitors (apocynin or diphenleneiodonium, DPI). Western blotting and Immunofluorescence were used to evaluate PPAR gammaexpression. Activation of NFkappaB was measured using transcription factor assay kit and Western blotting analysis of phospho-NFkappaB. PPARgamma expression was also tested in OIR and lipoploysaccharides-induced retinal inflammation. Results: Retinal expression of PPARgamma was suppressed in experimental models of diabetes, OIR and retinal inflammation. This was associated with activation of NFkappaB in diabetic retina. These effects were prevented by apocynin or deletion of NOX2. PPARgamma expression was also suppressed in endothelial cells treated with high glucose and this was prevented by apocynin, DPI and SOD. Conclusion: Suppression of PPARgamma is involved in the pathogenesis of diabetic retinopathy and OIR. NADPH oxidase could be an upstream mediator of these changes.




  
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Original Reference(s)
PPARGHumanExperimental Diabetes Mellitus  ISOPparg (Mus musculus)protein:decreased expression:retinaRGD 
PpargRatExperimental Diabetes Mellitus  ISOPparg (Mus musculus)protein:decreased expression:retinaRGD 
PpargMouseExperimental Diabetes Mellitus  IEP protein:decreased expression:retinaRGD 
PPARGHumanOxygen-Induced Retinopathy  ISOPparg (Mus musculus)protein:decreased expression:retina (mouse)RGD 
PpargRatOxygen-Induced Retinopathy  ISOPparg (Mus musculus)protein:decreased expression:retina (mouse)RGD 
PpargMouseOxygen-Induced Retinopathy  IEP protein:decreased expression:retina (mouse)RGD 


Genes (Rattus norvegicus)
Pparg  (peroxisome proliferator-activated receptor gamma)

Genes (Mus musculus)
Pparg  (peroxisome proliferator activated receptor gamma)

Genes (Homo sapiens)
PPARG  (peroxisome proliferator activated receptor gamma)