Contribution of impairment of redox-regulation in development of Intraretinal microvascular abnormalities

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Diabetic retinopathy(DR) is characterized by the development of intraretinal microvascular abnormalities. Endoplasmic reticulum(ER) stress is known to play a pathogenic role in vascular impairment in DR. Intravitreous injection of an ER stress inducer in mice increased the permeability of tracer dye across retinal blood vessels. The treatment of human retinal endothelial cells with ER stress inducers leads to the down-regulation of mainly claudin-5 among tight junction proteins, accompanied by elevation of retinal endothelial permeability. Moreover, p38 MAP kinase and subsequent NF-kB signaling pathways should contribute to the regulation of claudin-5 expression. The effects of dexamethasone are thought to be due to the transrepression of the above signaling and direct regulation of claudin-5 gene.