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Effect of lncRNA H19 on the apoptosis of vascular endothelial cells in arteriosclerosis obliterans via the NF-κB pathway

机译:lncRNA H19通过NF-κB通路对闭塞性动脉硬化血管内皮细胞凋亡的影响

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OBJECTIVE: To explore the effect of long non-coding ribonucleic acid (lncRNA) H19 on the apoptosis of vascular endothelial cells in arteriosclerosis obliterans (ASO) via the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway. PATIENTS AND METHODS: Human umbilical vein endothelial cells (HUVECs) were cultured, and lncRNA H19 was inhibited by Si-H9 and overexpressed by H19-OE. Then, the apoptosis rate was detected by flow cytometry, the target of lncRNA H19 was detected by dual luciferase reporter gene assay, and changes in the protein level were determined via Western blotting (WB). RESULTS: LncRNA H19 exhibited high expression in serum of patients with ASO, and compared with that in congeneric normal mice, the expression of lncRNA H19 in ASO mice rose. Besides, the proliferation ability of cells transfected with H19-OE was markedly strengthened, and H19-OE treatment could down-regulate the expression level of the apoptin, active cysteinyl aspartate-specific proteinase-3 (Caspase-3). In addition, lncRNA H19 bound to micro ribonucleic acid (miR)-19a in a targeted way. After lncRNA H19 was overexpressed, the expression of the NF-κB pathway key factors, p38 and p65, were notably increased, and the nuclear translocation of p65 was significantly enhanced after transfection with miR-19a. CONCLUSIONS: LncRNA H19 promotes the proliferation of vascular endothelial cells in ASO and inhibits the apoptosis of them via the NF-κB pathway.
机译:目的:通过激活的B细胞核因子κ轻链增强剂(NF-κB)探讨长链非编码核糖核酸(lncRNA)H19对闭塞性动脉硬化症(ASO)血管内皮细胞凋亡的影响。途径。病人与方法:培养人脐静脉内皮细胞(HUVECs),lncRNA H19被Si-H9抑制而被H19-OE过表达。然后,通过流式细胞术检测细胞凋亡率,通过双重荧光素酶报告基因测定法检测lncRNA H19的靶标,并通过蛋白质印迹法(WB)测定蛋白质水平的变化。结果:LncRNA H19在ASO患者血清中高表达,与同类小鼠相比,LncRNA H19在ASO小鼠中的表达升高。此外,转染H19-OE的细胞的增殖能力显着增强,并且H19-OE处理可下调凋亡素,活性半胱氨酸天冬氨酸特异性蛋白酶3(Caspase-3)的表达水平。另外,lncRNA H19以靶向方式与微核糖核酸(miR)-19a结合。过量表达lncRNA H19后,miR-19a转染后,NF-κB通路关键因子p38和p65的表达明显增加,p65的核转位明显增强。结论:LncRNA H19通过ASO促进血管内皮细胞的增殖,并通过NF-κB途径抑制其凋亡。

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