ATG16L1 promotes cell migration and invasion in high glucose-induced retinal capillary endothelial cells

Abstract

Background As a common chronic complication of diabetes, diabetic retinopathy (DR) often results in an irreversible visual dysfunction. ATG16L1 might be a potential biomarker of DR. Our study focused on the underlying mechanisms of Atg16L1 in diabetic retinopathy. Method In this study, we investigated the role of ATG16L1 in high glucose (HG)-induced retinal capillary endothelial cells (RCECs). Rat RCECs were cultured in normal glucose (NG) or high glucose (HG) medium with or without ATG16L1 transfection. Results First, the expression of ATG16L1 mRNA and protein was found to be significantly upregulated in RCECs exposed to HG. Moreover, the migration ability and invasion rate of RCECs in the high glucose group were considerably higher than those in the RCECs of the normal glucose group. The migration ability and invasion rate of RCECs in both normal and high glucose groups decreased significantly after transfection with ATG16L1 siRNA compared to migration and invasion of the RCECs in the control group (P < 0.01). Conclusion The results of this study indicated that ATG16L1 might be involved in the development of DR by promoting the migration of RCECs.