Abstract
ABSTRACT Long noncoding RNAs (LncRNAs) have been shown to play critical roles in the development of diabetic retinopathy (DR), which is often regarded as the most frequent cause of visual loss in the world. This study investigated the effect and mechanism of lncRNA taurine-upregulated gene 1 (TUG1) in DR. Quantitative real-time polymerase chain reaction (qRT-PCR) revealed that TUG1 was upregulated in streptozotocin (STZ)-induced rat model of DR and human retinal microvascular endothelial cells (hRMECs) incubated with high glucose (HG). TUG1 suppression decreased the proliferation, migration, and angiogenesis of HG-induced hRMECs. TUG1 sponges miR-524-5p, which is downregulated in hyperglycemia. Additionally, the fibroblast growth factor receptor 2 (FGFR2) was verified as a miR-524-5p target gene and was overexpressed in HG-treated hRMECs. More notably, overexpression of FGFR2 has been shown to significantly reduce the impact of miR-524-5p overexpression. Additionally, TUG1 silencing ameliorates diabetes mellitus-induced retinal vascular impairment in vivo. Taken together, suppressing TUG1 impairs vascular function in diabetic retinas via controlling miR-524-5p and FGFR2, suggesting a possible therapy method for DR.
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