Long non‑coding RNA MALAT1 is involved in retinal pigment epithelial cell damage caused by high glucose treatment.

Abstract

The present study aimed to explore the role of long non‑coding RNA metastasis associated lung adenocarcinoma transcript 1 (lncRNA MALAT1) in high glucose (HG)‑induced ARPE‑19 cell damage. ARPE‑19 cells were cultured and treated with HG (25mmol/l glucose). MALAT1 expression was silenced following transfection of small interfering RNA. Cell apoptosis was measured using flow cytometry. The cellular levels of reactive oxygen species (ROS), malondialdehyde and superoxide dismutase activity were all measured to examine oxidative stress. Gene expression levels of MALAT1 were determined by reverse transcription‑quantitative (RT‑q)PCR, while expression of tumor necrosis factor (TNF)‑α, monocyte chemotactic protein 1 (MCP‑1), intercellular cell adhesion molecule 1 (ICAM‑1) and vascular endothelial growth factor (VEGF) was detected using RT‑qPCR and western blotting. MALAT1 expression was markedly increased in ARPE‑19cells treated with HG. HG treatment caused increased apoptosis and elevated ROS‑induced stress in ARPE‑19 cells and these effects could be partly attenuated by MALAT1 knockdown. Increased gene expression levels of TNF‑α, MCP‑1, ICAM‑1 and VEGF induced by HG were also alleviated by MALAT1 inhibition. Therefore, lncRNA MALAT1 is the key factor in ARPE‑19 cell damage caused by HG and may be a promising therapeutic target for clinical DRtherapy. However, further studies are still required to reveal the detailed mechanisms underlying lncRNA MALAT1 function.