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

TL;DR

This study shows that ATG16L1 promotes cell migration and invasion in retinal cells under high glucose conditions, which may contribute to diabetic retinopathy.

Contribution

The study identifies ATG16L1 as a novel factor promoting retinal capillary endothelial cell migration in diabetic retinopathy.

Findings

ATG16L1 expression is significantly upregulated in retinal cells under high glucose conditions.

Knocking down ATG16L1 reduces cell migration and invasion in high glucose–treated retinal cells.

ATG16L1 may play a role in the progression of diabetic retinopathy.

Abstract

Diabetic retinopathy (DR), a common chronic complication of diabetes, often results in irreversible visual dysfunction. This study investigated the mechanisms underlying the expression of ATG16L1, a potential biomarker of DR.

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 HG medium with or without ATG16L1 transfection.

The mRNA and protein expression levels of ATG16L1 were significantly upregulated in RCECs exposed to HG medium. The migration ability and invasion rate of RCECs were significantly higher in the HG group than in the NG group but decreased markedly after transfection with ATG16L1 siRNA, compared with those in the control group (p < 0.01).

ATG16L1 might be involved in the development of DR by promoting the migration of RCECs.

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