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H.-O. Jun, Y. S. Yu, J. Kim, K. Park, J. Kim, K.-W. Kim; Inhibition of Protein Kinase C- Attenuates Blood-Retinal Barrier Breakdown in Diabetic Retinopathy. Invest. Ophthalmol. Vis. Sci. 2007;48(13):4981.
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To investigate the relationship between PKCΔ activation and tight junction proteins in blood-retina barrier breakdown of diabetic retinopathy.
In experimental mice models of diabetic retinopathy with or without intravitreal injection of rottrelin, PKCΔ inhibitor, retinal vascular leakage was evaluated through intravenous injection of FITC-dextran. Expression of Tight junction proteins such as ZO-1, ZO-2, and occludin were evaluated by immunohistochemistry and Western blotting. In human retinal endothelial cell, alteration of tight junction proteins and PKCΔ were measure by western blot analysis after treatment of rottrelin in AGE-treated cells.
In the retina of diabetic mice, rottrelin blocked retinal vascular leakage, and increased expression of tight junction proteins. AGE-treated cell resulted in elevation of PKCΔ activity and decrease of ZO-1, ZO-2, and occludin. Treatment of rottrelin significantly inhibited AGE-induced PKCΔ elevation, and increased expression of ZO-1, ZO-2, and occludin.
Our results suggest that the blood-retina barrier breakdown of diabetic retinopathy was regulated by PKCΔ activation. PKCΔ inhibitor could confer the protection from blood-retinal barrier breakdown in diabetic retinopathy
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