Gene ( IF 2.6 ) Pub Date : 2020-07-25 , DOI: 10.1016/j.gene.2020.144992 Qingshan Zeng 1 , Jia Liu 1
Background and aim
Diabetic retinopathy is a severe diabetic complication and a major cause of blindness. In this study, we explored the role of circ_0001879 in retinal vascular dysfunction under diabetic conditions.
Methods
Human retinal microvascular endothelial cells (HRMECs) were divided into normal glucose group (NG, 5.5 mmol/L d-glucose), high glucose group (HG, 25 mmol/L d-glucose), and osmotic control group (5.5 mmol/L d-glucose + 19.5 mmol/L mannitol). The expression of circ_0001879 and miR-30-3p was assessed via qRT-PCR. The circ_0001879/miR-30-3p roles in retinal vascular dysfunction were investigated through Cell Counting Kit-8 and Transwell assay. Bioinformatics analysis and luciferase reporter assays were applied to examine interactions between circ_0001879 and miR-30-3p in HRMECs.
Results
The relative circ_0001879 expression was remarkably increased in diabetic retinas group than that in the control group. Silencing circ_0001879 suppressed the proliferation and migration of HRMECs under high-glucose conditions. In addition, circ_0001879 acted as a binding platform and miRNA sponge for miR-30-3p. Circ_0001879 modulated the function of HRMECs via targeting miR-30-3p.
Conclusion
Silencing circ_0001879 inhibited the proliferation and migration of HRMECs under high-glucose conditions via modulating miR-30-3p, which might shed new light on a novel potentially marker and molecular therapeutic target for diabetic retinopathy.
中文翻译:
沉默circ_0001879通过调节miR-30-3p,可在高糖条件下抑制人视网膜微血管内皮细胞的增殖和迁移。
背景和目标
糖尿病性视网膜病是严重的糖尿病并发症,是失明的主要原因。在这项研究中,我们探讨了circ_0001879在糖尿病条件下在视网膜血管功能障碍中的作用。
方法
将人视网膜微血管内皮细胞(HRMEC)分为正常葡萄糖组(NG,5.5 mmol / L d-葡萄糖),高血糖组(HG,25 mmol / L d-葡萄糖)和渗透对照组(5.5 mmol / L)d-葡萄糖+ 19.5mmol / L甘露醇。通过qRT-PCR评估circ_0001879和miR-30-3p的表达。通过Cell Counting Kit-8和Transwell方法研究了circ_0001879 / miR-30-3p在视网膜血管功能异常中的作用。应用生物信息学分析和萤光素酶报告基因检测法检测HRMEC中circ_0001879与miR-30-3p之间的相互作用。
结果
糖尿病视网膜组相对circ_0001879的表达明显高于对照组。沉默circ_0001879可抑制高糖条件下HRMEC的增殖和迁移。另外,circ_0001879充当miR-30-3p的结合平台和miRNA海绵。Circ_0001879通过靶向miR-30-3p调节了HRMEC的功能。
结论
沉默circ_0001879通过调节miR-30-3p在高糖条件下抑制了HRMECs的增殖和迁移,这可能为糖尿病性视网膜病的新型潜在标志物和分子治疗靶标提供了新的思路。