{"title":"[Bioinformatic analysis of molecular mechanism of IL-17 in regulating ulcerative colitis].","authors":"Cuiling Wu, Chenxia Ren","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Objective To identify hub genes and key pathways in ulcerative colitis (UC) by bioinformatics. Methods The mRNA expression microarray GSE134025 related to ulcerative colitis was retrieved from Gene Expression Omnibus (GEO) database. The differentially expressed genes (DEGs) between ulcerative colitis samples and normal intestinal mucosal cells were screened by the R limma package, and then GO and KEGG pathway analysis was carried out. The protein-protein interaction (PPI) network was constructed by STRING database, and Cytoscape software was used to screen the hub genes in the PPI network. KEGG mapper was employed to mark the location of the hub genes in signal pathway. Results A total of 190 DEGs were screened, of which 147 were up-regulated and 43 were down-regulated. GO function enrichment showed hub genes were mainly involved in biological processes including inflammatory response and positive regulation of proliferation. Cellular component mainly enriched in membrane and plasma membrane, maintaining the molecular functions of mediating heparin binding and cytokines. KEGG analysis showed that the enriched pathways are mainly related to cytokine-cytokine receptor interaction, chemokine signaling pathway and other signal transduction pathway. Ten hub genes such as IL-6, CXCL8, CXCL10, CXCL1, CXCL9, ANXA1, IL-1β, CCL20, CXCL2, and CXCL11 were screened out of the PPI network, which were located downstream of the signaling pathway regulated by IL-17. Conclusion The 10 hub genes related to the risk of UC were likely to be regulated by IL-17 during the occurrence and development of UC.</p>","PeriodicalId":23737,"journal":{"name":"Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology","volume":"39 1","pages":"21-25"},"PeriodicalIF":0.0000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Objective To identify hub genes and key pathways in ulcerative colitis (UC) by bioinformatics. Methods The mRNA expression microarray GSE134025 related to ulcerative colitis was retrieved from Gene Expression Omnibus (GEO) database. The differentially expressed genes (DEGs) between ulcerative colitis samples and normal intestinal mucosal cells were screened by the R limma package, and then GO and KEGG pathway analysis was carried out. The protein-protein interaction (PPI) network was constructed by STRING database, and Cytoscape software was used to screen the hub genes in the PPI network. KEGG mapper was employed to mark the location of the hub genes in signal pathway. Results A total of 190 DEGs were screened, of which 147 were up-regulated and 43 were down-regulated. GO function enrichment showed hub genes were mainly involved in biological processes including inflammatory response and positive regulation of proliferation. Cellular component mainly enriched in membrane and plasma membrane, maintaining the molecular functions of mediating heparin binding and cytokines. KEGG analysis showed that the enriched pathways are mainly related to cytokine-cytokine receptor interaction, chemokine signaling pathway and other signal transduction pathway. Ten hub genes such as IL-6, CXCL8, CXCL10, CXCL1, CXCL9, ANXA1, IL-1β, CCL20, CXCL2, and CXCL11 were screened out of the PPI network, which were located downstream of the signaling pathway regulated by IL-17. Conclusion The 10 hub genes related to the risk of UC were likely to be regulated by IL-17 during the occurrence and development of UC.
目的用生物信息学方法鉴定溃疡性结肠炎(UC)的中心基因和关键通路。方法从Gene expression Omnibus (GEO)数据库中检索溃疡性结肠炎相关mRNA表达芯片GSE134025。通过R limma包筛选溃疡性结肠炎样本与正常肠粘膜细胞之间的差异表达基因(DEGs),然后进行GO和KEGG通路分析。利用STRING数据库构建蛋白-蛋白相互作用(PPI)网络,利用Cytoscape软件筛选PPI网络中的枢纽基因。利用KEGG作图器标记信号通路枢纽基因的位置。结果共筛选到190个基因,其中上调147个,下调43个。氧化石墨烯功能富集表明枢纽基因主要参与炎症反应和增殖正向调节等生物学过程。细胞成分主要富集于细胞膜和质膜,维持介导肝素结合和细胞因子的分子功能。KEGG分析显示,富集的通路主要与细胞因子-细胞因子受体相互作用、趋化因子信号通路及其他信号转导通路有关。从PPI网络中筛选出IL-6、CXCL8、CXCL10、CXCL1、CXCL9、ANXA1、IL-1β、CCL20、CXCL2和CXCL11等10个枢纽基因,它们位于IL-17调控的信号通路下游。结论与UC发生发展相关的10个枢纽基因可能在UC发生发展过程中受到IL-17的调控。