IL-10 inhibits retinal pigment epithelium cell proliferation and migration through regulation of VEGF in rhegmatogenous retinal detachment.

Abstract

Rhegmatogenous retinal detachment (RRD) is a disorder of the eye that affects physical and mental health. Retinal pigment epithelium (RPE) is closely associated with RRD, and it is hypothesized that RPE-secreted inflammatory cytokines may induce early pathological changes of RRD and may participate in RPE proliferation and migration. The present study determined a role for interleukin (IL)‑10 as an RPE‑secreted immune regulatory factor that contributes to RRD. A rat RRD model was established and RPE cells were isolated and cultivated. RPE cells were randomly divided into four groups, three treated with different concentrations of IL‑10 (100, 50, and 20mM) and one untreated. RPE cell proliferation was evaluated by MTT assay and the activity of caspase‑3 was also measured. RPE cell invasion was determined by Transwell assay. Vascular endothelial growth factor A (VEGF) expression was examined by reverse transcription‑quantitative polymerase chain reaction and western blotting; IL‑1 and IL‑6 levels were measured by ELISA. IL‑10 treatment suppressed RPE cell proliferation and migration, promoted caspase‑3 activity, inhibited VEGF mRNA and protein expression, and downregulated the secretion of inflammatory cytokines IL‑1 and IL‑6 in RRD group compared with the untreated Model group. The aforementioned effects of IL‑10 became more evident with increasing IL‑10 concentration. IL‑10 suppressed inflammation, facilitated RPE cell apoptosis and inhibited cell proliferation and migration through the regulation of VEGF expression.