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Identification of Differential Intestinal Mucosa Transcriptomic Biomarkers for Ulcerative Colitis by Bioinformatics Analysis

机译:生物信息学分析鉴定鉴别尿液粘膜转录组生物标志物的溃疡性结肠炎

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Background. Ulcerative colitis (UC) is a complicated disease caused by the interaction between genetic and environmental factors that affect mucosal homeostasis and triggers inappropriate immune response. The purpose of the study was to identify significant biomarkers with potential therapeutic targets and the underlying mechanisms. Methods. The gene expression profiles of GSE48958, GSE73661, and GSE59071 are from the GEO database. Differentially expressed genes (DEGs) were screened by the GEO2R tool. Next, the Database for Annotation, Visualization and Integrated Discovery (DAVID) was applied to analyze gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway. Then, protein-protein interaction (PPI) was visualized by Cytoscape with Search Tool for the Retrieval of Interacting Genes (STRING). Results. There were a total of 128 common DEGs genes, including 86 upregulated genes enriched in extracellular space, regulation of inflammatory response, chemokine-mediated signaling pathway, response to lipopolysaccharide, and cell proliferation, while 42 downregulated genes enriched in the integral component of the membrane, the integral component of the plasma membrane, apical plasma membrane, symporter activity, and chloride channel activity. The KEGG pathway analysis results demonstrated that DEGs were particularly enriched in cytokine-cytokine receptor interaction, TNF signaling pathway, chemokine signaling pathway, pertussis, and rheumatoid arthritis. 18 central modules of the PPI networks were selected with Cytotype MCODE. Furthermore, 18 genes were found to significantly enrich in the extracellular space, inflammatory response, chemokine-mediated signaling pathway, TNF signaling pathway, regulation of cell proliferation, and immune response via reanalysis of DAVID. Conclusion. The study identified DEGs, key target genes, functional pathways, and pathway analysis of UC, which may provide potential molecular targets and diagnostic biomarkers for UC.
机译:背景。溃疡性结肠炎(UC)是由影响粘膜稳态的遗传和环境因素之间的相互作用引起的复杂疾病,并触发不恰当的免疫应答。该研究的目的是鉴定具有潜在治疗目标和潜在机制的重要生物标志物。方法。 GSE48958,GSE73661和GSE59071的基因表达谱来自Geo数据库。通过GEO2R工具筛选差异表达基因(DEGS)。接下来,应用用于注释,可视化和集成发现(DavID)的数据库来分析基因本体(GO)和基因组(Kegg)途径的基因内科和京都百科全书。然后,通过Cytoskape通过Cytoskape可视化蛋白质 - 蛋白质相互作用(PPI),用于检索相互作用基因(串)。结果。总共有128个常见的参数基因,其中包含86个上调基因,富含细胞外空间,炎症反应的调节,趋化因子介导的信号通路,对脂多糖的反应,以及细胞增殖,而42个中间的基因富含在膜的整体组分中,血浆膜,顶端血浆膜,叙述活性和氯化物通道活性的整体组分。 KEGG途径分析结果表明,在细胞因子 - 细胞因子受体相互作用,TNF信号通路,趋化因子信号通路,百日咳和类风湿性关节炎中特别富集。使用细胞型MCODE选择PPI网络的18个中央模块。此外,发现18个基因在细胞外空间,炎症反应,趋化因子介导的信号通路,TNF信号通路,细胞增殖调节和通过大卫分析的免疫应答中的基因显着富集。结论。该研究确定了UC的次数,关键靶基因,功能途径和途径分析,其可以为UC提供潜在的分子靶标和诊断生物标志物。

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