LAUSR

Pericytes play a crucial role in preventing endothelial permeability by maintaining the integrity of tight junctions in endothelial cells; however, early pathological change in diabetic retinopathyis pericyte loss, which can lead to visual impairment by increasing endothelial permeability. Therefore, finding proteins and mechanisms that cause pericyte loss in diabetic retinopathy is beneficial for attenuating vision impairment. The present study focused on the effect of IL-1β on pericyte loss and endothelial permeability in diabetic retinopathy. It was demonstrated that IL-1β increased in the diabetic mouse retina and that the source of IL-1β could be endothelial cells and microglia. IL-1β induced pericyte apoptosis via NF-κB activation under high glucose conditions, but did not induce endothelial cell apoptosis. Moreover, IL-1β did not affect permeability in the endothelial cell monolayer; however, when cocultured with pericytes and endothelial cells, it increased endothelial cell permeability by reducing the amount of tight junction protein in endothelial cells. Furthermore, NF-κB inhibitor restored the altered permeability and tight junction protein expression in endothelial cells induced by IL-1β in cocultures of pericytes and endothelial cells. Collectively, IL-1β induced pericyte apoptosis via NF-κB activation under high glucose conditions, thereby increasing endothelial permeability in diabetic retinopathy. Blocking IL-1β/NF-κB signaling could be a promising therapeutic target to prevent pericyte loss in diabetic retinopathy.