Zhou Xing, Wu Lidong
Department of Orthopedic Surgery, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Orthopedics Research Institute of Zhejiang University, Hangzhou, Zhejiang, China.
Front Genet. 2023 Apr 6;14:1143644. doi: 10.3389/fgene.2023.1143644. eCollection 2023.
Synovial neovascularization is an early and remarkable event that promotes the development of rheumatoid arthritis (RA) synovial hyperplasia. This study aimed to find potential diagnostic markers and molecular therapeutic targets for RA at the mRNA molecular level. We download the expression profile dataset GSE46687 from the gene expression ontology (GEO) microarray, and used R software to screen out the differentially expressed genes between the normal group and the disease group. Then we performed functional enrichment analysis, used the STRING database to construct a protein-protein interaction (PPI) network, and identify candidate crucial genes, infiltration of the immune cells and targeted molecular drug. Rheumatoid arthritis datasets included 113 differentially expressed genes (DEGs) including 104 upregulated and 9 downregulated DEGs. The enrichment analysis of genes shows that the differential genes are mainly enriched in condensed chromosomes, ribosomal subunits, and oxidative phosphorylation. Through PPI network analysis, seven crucial genes were identified: RPS13, RPL34, RPS29, RPL35, SEC61G, RPL39L, and RPL37A. Finally, we find the potential compound drug for RA. Through this method, the pathogenesis of RA endothelial cells was further explained. It provided new therapeutic targets, but the relationship between these genes and RA needs further research to be validated in the future.
滑膜新生血管形成是促进类风湿性关节炎(RA)滑膜增生发展的早期且显著的事件。本研究旨在在mRNA分子水平上寻找RA的潜在诊断标志物和分子治疗靶点。我们从基因表达综合数据库(GEO)微阵列下载了表达谱数据集GSE46687,并使用R软件筛选出正常组和疾病组之间的差异表达基因。然后我们进行了功能富集分析,使用STRING数据库构建蛋白质-蛋白质相互作用(PPI)网络,并鉴定候选关键基因、免疫细胞浸润和靶向分子药物。类风湿性关节炎数据集包括113个差异表达基因(DEG),其中104个上调,9个下调。基因富集分析表明,差异基因主要富集在浓缩染色体、核糖体亚基和氧化磷酸化中。通过PPI网络分析,鉴定出七个关键基因:RPS13、RPL34、RPS29、RPL35、SEC61G、RPL39L和RPL37A。最后,我们找到了RA的潜在复合药物。通过这种方法,进一步解释了RA内皮细胞的发病机制。它提供了新的治疗靶点,但这些基因与RA之间的关系需要进一步研究以在未来得到验证。