贵州医科大学学报

2016, v.41;No.188(05) 507-510

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沉默干扰素诱导蛋白16对人主动脉外膜成纤维细胞凋亡的影响
Reducing Effect of IFI16 Expression on Human Aortic Adventitial Fibroblasts Apoptosis

肖燕;吴强;
XIAO Yan;WU Qiang;Department of Internal Medicine,Guizhou Medcial University;Department of Cardiology,Guizhou Province People's Hospital Affiliated to Guizhou Medcial University;

摘要(Abstract):

目的:探讨沉默干扰素诱导蛋白16(IFI16)表达对人主动脉外膜成纤维细胞(HAAFs)凋亡的影响及其部分机制。方法:应用IFI16小干扰RAN(siRNA)、Control siRNA转染HAAFs分别IFI16基因沉默组(IFI16-siRNA组)、阴性对照组(Control-siRNA组),未经干预的HAAFs作为空白组;用流式细胞仪检测凋亡,应用Western blot检测IFI16、细胞外调节蛋白激酶1/2(ERK1/2)、磷酸化ERK1/2(p-ERK1/2)蛋白表达。结果:与Control-siRNA组或空白组相比,IFI16-siRNA组的细胞凋亡率下降,伴随着IFI16蛋白表达减少,p-ERK1/2水平增高,差异有统计学意义(P<0.05)。结论:沉默IFI16表达可减少HAAFs细胞凋亡,其机制可能部分与ERK信号通路有关。
Objective: To investigate the effect of silencing interferon-inducible protein 16( IFI16)expression on the apoptosis of human aortic adventitial fibroblasts( HAAFs). Methods: The specific small interference RNAs( siRNAs) of IFI16 and Control siRNA were transected into HAAFs in IFI16-siRNA group,negative control group and untreated blank group. Cell apoptosis was analyzed by flow cytometry. The protein levels of IFI16,extracellular signal-regulated kinase( ERK1 /2) and phosphorylated extracellular signal-regulated kinase( p-ERK1 /2) were measured by Western Blot. Results:The protein expression levels of IFI16 were decreased in the HAAFs,the cell apoptosis was downregulated,the protein expression levels of p-ERK1 /2 were increased,differences were statistic significant( P < 0. 05). Conclusion: Inhibition of IFI16 expression can downregulate HAAFs cell apoptosis,which may be related to the ERK signaling pathway.

关键词(KeyWords): 干扰素诱导蛋白;血管外膜成纤维细胞;凋亡
interferon-inducible protein;human aortic adventitial fibroblasts;apoptosis

Abstract:

Keywords:

基金项目(Foundation): 国家自然科学基金资助项目(81260030);; 贵州省科学技术厅-贵州省人民医院科技联合基金项目[黔科合LH字(2015)7159号]

作者(Author): 肖燕;吴强;
XIAO Yan;WU Qiang;Department of Internal Medicine,Guizhou Medcial University;Department of Cardiology,Guizhou Province People's Hospital Affiliated to Guizhou Medcial University;

Email:

DOI: 10.19367/j.cnki.1000-2707.2016.05.003

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