基于生物信息学分析癫痫脑内星形胶质细胞炎性激活机制  被引量:3

The inflammatory mechanism of activated astrocyte in epileptic brain based on bioinformatics analysis

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作  者:梁沛余 雷有芳 张景宣 吴穹[1] LIANG Pei-yu;LEI You-fang;ZHANG Jing-xuan;WU Qiong(College of Medicine,Qinghai Unitersity,Xining,Qinghai 810001,China;不详)

机构地区:[1]青海大学医学院,青海西宁810001 [2]武汉大学基础医学院

出  处:《现代预防医学》2020年第23期4385-4389,共5页Modern Preventive Medicine

基  金:国家自然科学基金资助项目(81860762);青海省2018年科技计划基础研究计划项目(2018-ZJ-721);青海省卫生计生科研指导性计划课题(2018-wjzdx-131)。

摘  要:目的挖掘癫痫脑内星形胶质细胞异常炎性激活的关键信号分子,为进一步阐明神经免疫促痫机理提供生物信息学基础。方法 NCBI GEO数据库获取癫痫动物模型(GSE73878)和星形胶质细胞炎性激活细胞模型(GSE73022)基因芯片结果,GEO2R在线筛选共有差异表达基因(DEGs),DAVID数据库进行GO功能模块和KEGG通路富集分析,STRING数据库和Cytoscape软件构建DEGs蛋白质互作网络,多算法筛选Hub基因,最后利用GEPIA数据库在易发癫痫的低级别胶质瘤患者中验证。结果两芯片交集共获得72个DEGs,主要富集在调控免疫反应、细胞因子活力等过程,病毒感染类似信号、Toll样受体信号等通路;59个基因可构成大的蛋白互作网络,其中24个基因组成核心模块,多算法筛选结合GEIPA数据库发现Gbp3、Ifit3、Irf7、Stat1是Hub基因。结论癫痫脑内星形胶质细胞异常炎性激活与Gbp3、Ifit3、Irf7、Stat1等基因关系密切,其可能是调控癫痫脑内神经免疫促痫过程的新靶点。Objective To explore the key signal molecules of inflammatory astrocyte in epileptic brain,so as to provide bioinformatics basis for further research of the neuro-immune regulated mechanism.Methods Two GeneChips(GSE73878;GSE73022)containing animal model and cellular model were obtained from NCBI GEO Datasets.GEO2 R and DAVID were used to analyze the DEGs and its enrichment in GO and KEGG.Then,the PPI network was built to screen Hub genes by STRING and Cytoscape.GEPIA was used to verify Hub genes in patients with Low grade glioma.Results A total of 72 DEGs were screened out,and they mainly enriched in immune system process,cytokine activity,virus-like infection pathway and Toll-like receptor signal.The biggest PPI model consisted of 59 genes which contained multiple core modules,and four Hub genes were screened out,including Gbp3,Ifit3,Irf7,Stat1.Conclusion The inflammatory mechanism of activated astrocyte in epileptic brain is associated with Gbp3,Ifit3,Irf7,Stat1,and these Hub genes maybe new targets for neuro-immune regulation.

关 键 词:癫痫 星形胶质细胞 生物信息学 新靶点 

分 类 号:R113[医药卫生—公共卫生与预防医学] R742.1

 

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