Targeting long non-coding RNA RP11-502I4.3 delays the trend of angiogenesis in diabetic retinopathy

Based on our previous findings, we hypothesized that the long non-coding RNA RP11-502I4.3 may be involved in angiogenesis associated with Diabetic retinopathy (DR). We investigated the role of RP11-502I4.3 in DR by examining its regulation of vascular endothelial growth factor (VEGF). We assessed differences in RP11-502I4.3 expression between the normal control group and streptozotocin-induced diabetic rats or high glucose (HG)-stimulated human retinal microvascular endothelial cells (HRMECs). VEGF expression was measured with and without lentiviral vectors overexpressing RP11-502I4.3. We analyzed the structural and functional alterations related to DR. Our analysis revealed that RP11-502I4.3 expression was lower in the retinas of diabetic rats and in HG-stimulated HRMECs compared with normal glucose conditions. Overexpressing of RP11-502I4.3 resulted in decreased VEGF levels. Diabetic rats exhibited retinopathy characterized by thinning of the retinal layer thickness, structural changes in the inner and outer nuclear layers, a reduced count of retinal ganglion cells, and the presence of acellular capillaries. The proliferative activity, migration count, and tube formation ability of HG-treated HRMECs were significantly higher than those of the normal control group; however, these changes were delayed by RP11-502I4.3 overexpression. RP11-502I4.3 downregulation in DR appears to promote angiogenesis.