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 20 mM) 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.