Dexamethasone reverses the effects of high glucose on human retinal endothelial cells in vitro

Purpose Diabetic retinopathy is the leading cause of preventable blindness in the working population and its prevalence continues to increase as the worldwide prevalence of diabetes grows. The main cause of visual loss in diabetic eye disease is diabetic macular oedema caused by an increase in microvascular endothelial permeability. Endothelial cell permeability is influenced by multiple factors which have not been fully elucidated, particularly in human models. Inflammation has been reported in the pathogenesis of diabetic retinopathy and the potential use of anti-inflammatory agents such as the glucocorticoid dexamethasone is being extensively studied. Methods The effect of high glucose (25 mM) and dexamethasone on retinal endothelial cell proliferation and permeability were assessed using Cell-8 proliferation reagent and passage of Evan's blue albumin, respectively. qPCR was used to quantify gene expression of selected tight junction molecules (Occludin, Claudin-5, JAM-A and JAM-C) and adheren junction (VE-Cadherin) molecules with high glucose and dexamethasone. Results High glucose decreased endothelial cell proliferation and this effect was reversed by dexamethasone. High glucose conditions significantly increased endothelial cell permeability and this effect was decreased with dexamethasone treatment for 24 and 72 hours. In retinal endothelial cell exposed to high glucose claudin-5, occludin and JAM-A gene expression were reduced and that of JAM-C increased when evaluated with qPCR; dexamethasone was effective in partially reversing these changes. Conclusions Dexamethasone reverses high glucose induced alterations in retinal endothelial cell behaviour.