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Advanced Glycation End Products Induce Blood–Retinal Barrier Dysfunction in Normoglycemic Rats

Stitt, AW, Bhaduri, T, Moore, Tara, Connolly, J, Gardiner, TA and Archer, DB (2000) Advanced Glycation End Products Induce Blood–Retinal Barrier Dysfunction in Normoglycemic Rats. Molecular Cell Biology Research Communications, 3 . [Journal article]

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DOI: doi:10.1006/mcbr.2000.0243


Advanced glycation end products (AGEs) have been implicated in the progressive vascular dysfunction which occurs during diabetic retinopathy. In the current study we have examined the role of these adducts in blood–retinal barrier (BRB) breakdown and investigated expression of the vasopermeabilizing agent vascular endothelial growth factor (VEGF) in the retina. When normoglycemic rats were injected with AGE-modified albumin daily for up to 10 days there was widespread leakage of FITC-dextran and serum albumin from the retinal vasculature when compared to control animals treated with nonmodified albumin. Ultrastructural examination of the vasculature revealed areas of attenuation of the retinal vascular endothelium and increased vesicular organelles only in the AGE-exposed rats. Quantitative RT-PCR and in situ hybridization demonstrated a significant increase in retinal VEGF mRNA expression (P < 0.05). These results suggest that AGEs can initiate BRB dysfunction in nondiabetic rats and a concomitant increase in retinal VEGF expression. These findings may have implications for the role of AGEs in the pathogenesis of diabetic retinopathy. Author Keywords: vascular endothelial growth factor; retina; diabetic retinopathy; advanced glycation end products; blood–retinal barrier

Item Type:Journal article
Faculties and Schools:Faculty of Life and Health Sciences
Faculty of Life and Health Sciences > School of Biomedical Sciences
Research Institutes and Groups:Biomedical Sciences Research Institute
Biomedical Sciences Research Institute > Genomic Medicine
ID Code:4095
Deposited By: Professor Tara Moore
Deposited On:18 Dec 2009 14:53
Last Modified:23 May 2017 14:03

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