[1]李伟华,安书杰,孟 华,等.circFAM73A靶向调控miR-140-3p对高糖诱导人视网膜血管内皮细胞凋亡、迁移和炎症因子释放的影响[J].陕西医学杂志,2023,52(11):1451-1457.[doi:DOI:10.3969/j.issn.1000-7377.2023.11.001]
 LI Weihua,AN Shujie,MENG Hua,et al.Effects of circFAM73A targeting miR-140-3p on apoptosis,migration and inflammatory factor release of human retinal vascular endothelial cells induced by high glucose[J].,2023,52(11):1451-1457.[doi:DOI:10.3969/j.issn.1000-7377.2023.11.001]
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circFAM73A靶向调控miR-140-3p对高糖诱导人视网膜血管内皮细胞凋亡、迁移和炎症因子释放的影响
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《陕西医学杂志》[ISSN:1000-7377/CN:61-1281/TN]

卷:
52
期数:
2023年11期
页码:
1451-1457
栏目:
基础研究
出版日期:
2023-11-05

文章信息/Info

Title:
Effects of circFAM73A targeting miR-140-3p on apoptosis,migration and inflammatory factor release of human retinal vascular endothelial cells induced by high glucose
作者:
李伟华1安书杰1孟 华1沙南希1王双勇2
(1.空军军医大学西京医院综合诊疗科,陕西 西安 710032; 2.广州医科大学附属第三医院眼科,广东 广州 510150)
Author(s):
LI WeihuaAN ShujieMENG HuaSHA NanxiWANG Shuangyong
(Department of Comprehensive Diagnosis and Treatment,Xijing Hospital of Air Force Medical University,Xi'an 710032,China)
关键词:
人视网膜血管内皮细胞 circFAM73A miR-140-3p 细胞凋亡 细胞迁移 炎症因子
Keywords:
Human retinal vascular endothelial cell circFAM73A miR-140-3p Apoptosis Cell migration Inflammatory cytokine
分类号:
R 774
DOI:
DOI:10.3969/j.issn.1000-7377.2023.11.001
文献标志码:
A
摘要:
目的:探讨circFAM73A靶向调控miR-140-3p对高糖诱导的人视网膜血管内皮细胞凋亡、迁移和炎症因子释放的影响及作用机制。方法:将人视网膜血管内皮细胞分别采用5.5 mmol/L葡萄糖(NG组)或25 mmol/L葡萄糖(HG组)处理,在HG组分别转染si-circRNA FAM73A和miR-140-3p inhibitors后,RT-qPCR检测circRNA FAM73A、miR-140-3p、TNF-α和IL-6表达水平; 流式细胞术和Western blot分别检测细胞凋亡情况和凋亡相关分子Cleaved caspase 3的表达水平; Transwell检测细胞迁移情况; 双荧光素酶报告实验与RIP检测circRNA FAM73A和miR-140-3p的靶向结合情况。结果:circFAM73A的表达水平在高糖处理人视网膜血管内皮细胞后显著升高,miR-140-3p的表达水平显著下降(均P<0.05); 沉默circFAM73A能够显著抑制高糖诱导的人视网膜血管内皮细胞凋亡、迁移、炎症因子TNF-α和IL-6的释放(均P<0.05); 低表达miR-140-3p能够显著促进高糖诱导的人视网膜血管内皮细胞凋亡、迁移、炎症因子TNF-α和IL-6的释放(均P<0.05); 双荧光素酶报告和RIP实验证实circRNA FAM73A能够靶向结合miR-140-3p; 共转染si-circRNA FAM73A和miR-140-3p inhibitors能够显著减弱低表达miR-140-3p对人视网膜血管内皮细胞凋亡、迁移和炎症因子释放的作用(均P<0.05)。结论:沉默circFAM73A能够通过靶向结合miR-140-3p抑制高糖诱导的人视网膜血管内皮细胞凋亡、迁移和炎症因子释放。
Abstract:
Objective:To investigate the effects and specific mechanisms of circFAM73A targeting regulation of miR-140-3p on high glucose-induced human retinal vascular endothelial cell apoptosis,migration and inflammatory cytokine release.Methods:Human retinal vascular endothelial cells were treated with 5.5 mmol/L glucose(control group,NG group)or 25 mmol/L glucose(high glucose group,HG group),and then transfected with si-circRNA FAM73A and miR-140-3p inhibitors in the HG group.The expression levels of circRNA FAM73A,miR-140-3p,TNF-α,and IL-6 were detected by RT-qPCR.Flow cytometry and Western blot were used to detect cell apoptosis and the expression levels of apoptosis-related molecule Cleaved caspase 3.Transwell assay was performed to detect cell migration.Dual-luciferase reporter assay and RNA immunoprecipitation(RIP)were used to detect the targeting binding of circRNA FAM73A and miR-140-3p.Results:The expression level of circFAM73A was significantly increased in human retinal vascular endothelial cells treated with high glucose(P<0.05),while the expression level of miR-140-3p was significantly decreased(P<0.05).Silencing circFAM73A could significantly inhibit high glucose-induced cell apoptosis,migration,and release of inflammatory cytokines TNF-α and IL-6 in human retinal vascular endothelial cells(all P<0.05).Low expression of miR-140-3p could significantly promote high glucose-induced cell apoptosis,migration,and release of inflammatory cytokines TNF-α and IL-6 in human retinal vascular endothelial cells(all P<0.05).Dual-luciferase reporter assay and RIP confirmed that circRNA FAM73A could target bind to miR-140-3p.Co-transfection of si-circRNA FAM73A and miR-140-3p inhibitors could significantly attenuate the effects of low expression of miR-140-3p on cell apoptosis,migration,and inflammatory cytokine release in human retinal vascular endothelial cells(all P<0.05).Conclusion:Silencing circFAM73A can inhibit high glucose-induced apoptosis,migration,and release of inflammatory cytokines in human retinal vascular endothelial cells by targeting binding to miR-140-3p.

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备注/Memo

备注/Memo:
基金项目:国家自然科学基金资助面上项目(81200659)
更新日期/Last Update: 2023-11-06