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Hyoung Oh Jun, Jin Hyoung Kim, Young S. Yu, Jeong Hun Kim; Blockade Of Protein Kinase C Attenuates Blood-retinal Barrier Breakdown In Diabetic Retinopathy. Invest. Ophthalmol. Vis. Sci. 2012;53(14):5407.
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Vision loss in diabetic retinopathy is due to macular edema characterized by increased vascular permeability, which involves phosphorylation associated with activation of protein kinase C (PKC) isoforms. In this study, we demonstrated blockade of PKC ζ could prevent blood-retinal barrier breakdown in diabetic retinopathy.
Using streptozotocin-induced diabetic mice and vascular endothelial growth factor (VEGF)-treated human retinal microvascular endothelial cells (HRMECs), effect of PKC ζ inhibition on vascular permeability and tight junction protein expression was investigated through western blotting, RT-PCR, fluorescein angiography and immunohistochemistry.
Increased vascular permeability of diabetic retina is accompanied by a decrease of zonula occludens (ZO)-1 and ZO-2 expression. In diabetic retina and VEGF-treated human retinal microvascular endothelial cells, vascular leakage and loss of ZO-1 and ZO-2 on retinal vessels were effectively restored or prevented with treatment of PKC ζ inhibitor, transfection of siRNA for PKC ζ.
PKC ζ activation is involved in vascular permeability in response to diabetes, and inhibition of PKC ζ effectively restores loss of tight junction proteins in retinal vessels. Therefore, we suggest that inhibition of PKC ζ could be an alternative treatment to blood-retinal barrier breakdown in diabetic retinopathy
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