Zhai Kaihua, Kong Xiangli, Liu Boyu, Lou Jiyu
Department of Internal Neurology, Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Neurology Department, The First Affiliated Hospital of Xi'an Medical University, Xi'an, Shanxi Province, China Department of Endocrinology, Third Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan, People's Republic of China.
Medicine (Baltimore). 2017 Aug;96(34):e7564. doi: 10.1097/MD.0000000000007564.
This study aimed to identify the key differentially expressed genes (DEGs) following ischemic stroke (IS).The GSE22255 microarray dataset, which contains samples from peripheral blood mononuclear cells of 20 IS patients and 20 sex- and age-matched controls, was downloaded from the Gene Expression Omnibus. After data pre-processing, DEGs were identified using the Linear Models for Microarray Data package in R. The Search Tool for the Retrieval of Interacting Genes database was used to predict the interactions among the products of DEGs, and then Cytoscape software was used to visualize the protein-protein interaction (PPI) network. DEGs in the PPI network were then analyzed using the Database for Annotation, Visualization, and Integrated Discovery online software to predict their underlying functions through functional and pathway enrichment analyses.A total of 144 DEGs were identified in IS samples compared with control samples, including 75 upregulated and 69 downregulated genes. Genes with higher degrees in the PPI network included FOS (degree = 26), TP53 (degree = 22), JUN (degree = 20), EGR1 (degree = 18), JUNB (degree = 16), and ATF3 (degree = 15), and these genes may function in IS by interacting with each other (e.g., EGR1-JUN, EGR1-TP53, ATF3-FOS, and JUNB-FOS). Functional enrichment analysis indicated that the downregulated TP53 gene was enriched in immune response and protein targeting categories.ATF3 and EGR1 may have an important protective effect on IS, whereas FOS, JUN, and JUNB may be associated with the development of IS. In addition, TP53 may function as an indicator of poor prognosis for IS through its association with the immune response and protein targeting.
本研究旨在鉴定缺血性中风(IS)后的关键差异表达基因(DEG)。从基因表达综合数据库下载了GSE22255微阵列数据集,该数据集包含20例IS患者以及20例性别和年龄匹配的对照者的外周血单核细胞样本。经过数据预处理后,使用R语言中的微阵列数据线性模型软件包鉴定DEG。利用检索相互作用基因数据库预测DEG产物之间的相互作用,然后使用Cytoscape软件可视化蛋白质-蛋白质相互作用(PPI)网络。随后,使用在线软件注释、可视化和综合发现数据库对PPI网络中的DEG进行分析,通过功能和通路富集分析预测其潜在功能。与对照样本相比,在IS样本中总共鉴定出144个DEG,包括75个上调基因和69个下调基因。PPI网络中度数较高的基因包括FOS(度数=26)、TP53(度数=22)、JUN(度数=20)、EGR1(度数=18)、JUNB(度数=16)和ATF3(度数=15),这些基因可能通过相互作用在IS中发挥作用(例如,EGR1-JUN、EGR1-TP53、ATF3-FOS和JUNB-FOS)。功能富集分析表明,下调的TP53基因在免疫反应和蛋白质靶向类别中富集。ATF3和EGR1可能对IS具有重要的保护作用,而FOS、JUN和JUNB可能与IS的发展有关。此外,TP53可能通过与免疫反应和蛋白质靶向的关联而作为IS预后不良的指标。