类风湿关节炎基因差异谱的生物信息学分析

目的通过生物信息学方法探究类风湿关节炎患者的滑膜成纤维细胞差异表达基因及相关信号通路,寻找潜在的类风湿关节炎特异性分子标志物。方法利用R语言limma包等程序方法分析基因芯片GSE21959并筛选差异基因(differentially expressed genes,DEGs),利用DAVID数据库分析DEGs获得其GO富集分析和KEGG信号通路分析的结果。利用STRING数据库构建蛋白互作网络,再将结果导入Cytoscape软件中模块化核心基因并绘制蛋白互作网络图。结果筛选获得了123个差异基因,其中表达上调的基因38个,表达下调的基因85个。GO富集分析表明DEGs主要参与了趋化因子调节、CXCR趋化因子受体结合和血管生成正向调控等生物学过程,KEGG信号通路富集分析主要包括了趋化因子信号通路、Rap1信号通路和血管平滑肌收缩等信号通路。模块化分析获得了7个核心基因分别为:CXCL1、CXCL8、CXCL6、ADRA2A、ADCY8、S1PR1和SAA1。结论通过生物信息学分析获得类风湿关节炎的DEGs、核心基因、生物学过程和信号通路等信息,为探究类风湿关节炎的发病机制、发现诊断标志物和探索新治疗靶点提供理论依据与新的方向。

Bioinformatics analysis of the genetic difference spectrum of rheumatoid arthritis

Objective:To explore the differentially expressed genes,associated signaling pathways in synovial fibroblasts of patients with rheumatoid arthritis(RA)and to identify potential RA-specific molecular markers by using bioinformatics methods.Methods:R software was used to analyze the gene chip GSE65391 and screen the differentially expressed genes(DEGs).The DAVID database was used to analyze the DEGs to obtain the results of GO enrichment analysis and KEGG signal pathway analysis.The STRING database was used to construct a protein interaction network,and the results were imported into Cytoscape software to screen the core genes and map the protein interaction network.Results:A total of 123 differential genes were obtained,of which 38 genes were up-regulated and 85 gene was down-regulated.The GO enrichment analysis indicated that DEGs mainly participated in biological processes such as chemokine regulation of CXCR chemokine receptor binding and positive regulation of angiogenesis.The enrichment analysis of KEGG signaling pathways mainly included the chemokine signaling pathway Rap1 signaling pathway and vascular smooth muscle contraction and other signaling pathways.Finally,seven hub genes were screened for CXCL1,CXCL8,CXCL6,ADRA2A,ADCY8,S1PR1 and SAA1.Conclusion:Through bioinformatics analysis,information such as DEGs,hub genes,biological processes and signaling pathways of RA were obtained,which provided a theoretical basis and a new direction for exploring the pathogenesis of RA,discovering diagnostic markers and exploring drug therapeutic targets.