The Molecular Mechanism of Long Non-Coding RNA (LncRNA) Regulation of Notch Signaling in Glucose-Induced Apoptosis of Human Retinal Vascular Endothelial Cell

Abstract

Diabetes, a global health concern, affects the health of more than 500 million adults. The absence of Notch protein can cause an imbalance in the retinal vascular environment and cause retinal vascular disease. Long noncoding RNA (lncRNA) is known to be involved in the regulation of many signaling pathways. We hope to understand the specific mechanism of apoptosis in retinal vascular endothelial cells (RVECs) by exploring the regulatory effect of lncRNA on the Notch pathway. In this study, we found that RVECs treated with glucose showed increased levels of Notch transcript and protein expression. The lentiviral interference with Notch RNAi reversed this response. When Notch activity decreased, oxidative stress also decreased, accompanied by increased levels of Caspase-9 and Caspase-3 and an increased rate of apoptosis. Therefore, we believe that Notch is involved in the development of diabetic retinopathy and loss of expression promotes apoptosis of human RVECs. By inhibiting the Notch pathway, lncRNA promotes apoptosis of human RVECs in a high-glucose environment.