This retrospective case–control study examined the association between the rs2071559 (-604T/C) single nucleotide polymorphism (SNP) in the vascular endothelial growth factor receptor (VEGFR)-2 gene and the risk of diabetic retinopathy (DR) in Northern Han Chinese. This study included patients diagnosed with diabetes mellitus (DM) in Shijiazhuang between 07/2014 and 07/2016. The healthy controls were unrelated individuals who received routine physical examinations. The diabetic patients were grouped as DM (diabetes but no fundus examination abnormalities), proliferative DR (PDR), and non-proliferative DR (NPDR). Finally, 438 patients were included: 114 controls and 123, 105, and 96 patients in the DM, NPDR, and PDR groups, respectively. In the multivariable analyses and all genetic models, the VEGFR-2 rs2071559 SNP was not associated with DR (among all diabetic patients) or with PDR (among the patients with DR) after adjustment for age, sex, duration of DM, blood glucose, systolic blood pressure, diastolic blood pressure, and body mass index (all P > 0.05). In conclusion, the VEGFR-2- 604T/C rs2071559 SNP is not associated with DR or PDR in the Han Chinese population of Shijiazhuang (China).
Purpose: To investigate the effects of circ_0001953/miR-186 on human retinal vascular endothelial cell (HRVEC) injury evoked by high glucose. Methods: A cell model (HG group) was established using high glucose-treated HRVECs, while untreated HRVECs were used as the control group (Con group). The levels of endothelin-1 (ET-1), ICAM-1 and IL-6 were evaluated by ELISA and the content of malondialdehyde (MDA) and superoxide dismutase (SOD) in HRVECs were determined. Apoptosis rate was tested adopting flow cytometry. The interrelationship between circ_0001953 and miR-186 was assessed using dual luciferase reporter assay. Measurement of Bax and Bcl-2 was implemented via western blot. Results: In HG group, circ_0001953 increased while miR-186 was downregulated, ET-1, IL-6, ICAM-1, and apoptosis rate increased and accompanied with up-regulated Bax content and declined Bcl-2 protein level. Furthermore, the content of MDA increased and SOD decreased. MiR-186 was a target of circ_0001953. Conclusion: Inhibition of circ_0001953 can repress inflammation, oxidative stress and apoptosis in HRVECs by up-regulating the expression of miR-186.
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