Abstract
Purpose: :
The purpose of this study was to investigate role of clusterin on the alteration of tight junction proteins in Blood-retina barrier breakdown of diabetic retinopathy.
Methods: :
Advanced glycation end product (AGE)-treated human retina endothelial cells were cultured in the presence or absence of exogenous clusterin. Western blot analysis was used to analyze ZO-1 and ZO-2 tight junction proteins levels. Retinal vascular leakage was assessed using fluorophotometric dextran leakage assay. Streptozotocin-induced diabetic mice were injected with clusterin and examined vascular leakage.
Results: :
AGE-treated cell resulted in decrease of ZO-1, ZO-2. Addition of clusterin significantly increased ZO-1 and ZO-2 levels. There was widespread leakage of FITC-dextran in streptozotocin-induced diabetic mice. However, attenuation of vascular leakage was shown in clusterin treated mice.
Conclusions: :
The results from this study showed that the blood-retina barrier breakdown of diabetic retinopathy was regulated by clusterin. Clusterin could reverse the blood-retinal barrier breakdown.
Keywords: diabetic retinopathy • retinal degenerations: cell biology • drug toxicity/drug effects