系统性红斑狼疮患者PBMCs差异表达基因m6A修饰的生物信息学分析  

Bioinformatics analysis of N6⁃methyladenosine modifications of differential expression gene in PBMCs from systemic lupus erythematosus

作　　者：王晶 董辉[2] 党洁 霍正浩 马占兵 WANG Jing;DONG Hui;DANG Jie;HUO Zhenghao;MA Zhanbing(Department of Pathology,General Hospital of Ningxia Medical University,Yinchuan 750004,China;Medical Science Research Institute,General Hospital of Ningxia Medical University,Yinchuan 750004,China;Department of Cell Biology and Medical Genetics,Ningxia Medical University,Yinchuan 750004,China)

机构地区：[1]宁夏医科大学总医院病理科,银川750004 [2]宁夏医科大学总医院医学科学研究院,银川750004 [3]宁夏医科大学基础医学院医学遗传学与细胞生物学系,银川750004

出　　处：《生物信息学》2024年第3期183-191,共9页Chinese Journal of Bioinformatics

基　　金：国家自然科学基金项目(No.82060301);宁夏医科大学校级项目(No.XM2021075);校级特殊人才启动项目(No.XT2018018)

摘　　要：采用生物信息学方法,通过公共数据库,分析系统性红斑狼疮(SLE)N6-甲基腺苷(m6A)修饰谱系。基于公共数据建立SLE m6A传修饰表达谱,分析m6A相关的DEGs在SLE中的潜在作用;利用ADEx数据库获取DEGs,利用m6A GEO数据集(GSE173312),分析获取SLE m6A修饰谱;用DAVID对m6A DEGs进行GO/Pathway注释分析。在SLE患者中,m6A组分写入器RBM15B和擦除酶FTO的表达下调,阅读器IGFBP3的表达上调。SLE m6A修饰谱包括181个基因,其中123个基因的表达上调,58个基因的表达下调。这些基因主要参与了细胞凋亡和细胞周期通路、I型干扰素信号通路,DNA复制和B细胞MHC II分子调节等生物学过程。SLE患者的PBMCs细胞m6A修饰存在异常,并可能参与疾病的发生和发展。To analyze the N6⁃methyladenosine(m6A)modification profile in systemic lupus erythematosus(SLE)using bioinformatics methods and public databases.We establish an SLE m6A modification expression profile and analyze the potential roles of m6A⁃related differentially expressed genes(DEGs)in SLE using public data.DEGs are obtained from the ADEx database,and the m6A modification profile in SLE is analyzed using the m6A GEO dataset(GSE173312).Additionally,we perform GO/Pathway annotation analysis of m6A DEGs using DAVID.In SLE patients,the expression of the m6A writer components RBM15B and the eraser enzyme FTO are downregulated,while the expression of the reader IGFBP3 is upregulated.The SLE m6A modification profile include 181 genes,with 123 genes upregulated and 58 genes downregulated in expression.These genes are primarily involved in biological processes such as cell apoptosis and cell cycle pathways,type I interferon signaling pathway,DNA replication,and B cell MHC II molecule regulation.Abnormalities in PBMCs cell m6A modification are observed in SLE patients and may potentially contribute to the development and occurrence of the disease.

关 键 词：系统性红斑狼疮 N6-腺苷酸甲基化 差异表达 基因 生物标志物 

分 类 号：Q753[生物学—分子生物学]