Diabetic Retinopathy

UCA1[LncRNA]

miR-624-3p[miRNA]

VEGF[mRNA]

human retinal endothelial cells

Homo sapiens (human)

Biosci Rep. 2021 Jun 25;41(6):BSR20201389. doi: 10.1042/BSR20201389.

Long noncoding RNA UCA1 promotes high glucose-induced human retinal endothelial cells angiogenesis via regulating miR-624-3p/VEGF-C.

microarray;RT-PCR;Luciferase reporter assay;

AIMS/INTRODUCTION: Emerging evidences have indicated that lncRNAs play important roles in the development and progression of Diabetic retinopathy (DR). It is reported that UCA1 was highly expressed in diabetic lymphoendothelial cells and influences glucose metabolism in rats with DR. The aim of the present study was to explore the role of UCA1 in the mechanism of DR. METHODS: Gene expression analyses in fibrovascular membranes excised from patients with DR using public microarray datasets (GSE60436). RT-PCR was performed to detect UCA1, miR-624-3p and VEGF-C expressions in blood of patients and human retinal endothelial cells (HRECs). Moreover, CCK-8, transwell assay, and tube formation assay were used to identify biological effects of UCA1 on HRECs proliferation, migration ability and angiogenesis in vitro. RESULTS: UCA1 and VEGF-C was elevated in DR patients and high glucose-induced HRECs cell lines, while miR-624-3p was decreased. UCA1 inhibition inhibited proliferation, angiogenesis and migration of HRECs cells under high glucose condition. Luciferase reporter assay indicated that UCA1 could sponge with miR-624-3p, which could directly target at VEGF-C. Finally, we proved a pathway that UCA1 promoted cell proliferation, migration and angiogenesis through sponging with miR-624-3p thereby upregulating VEGF-C in high glucose-induced HRECs. CONSLUSIONS: We identified UCA1 as an important factor associated with DR, which could regulate the expression of VEGF-C by sponging miR-624-3p in human retinal endothelial cells. Our results pay the way for further studies on diagnostic and therapeutic studies related to UCA1 in DR patients.