Potential Biological Molecules and Immune Cell for Rheumatoid Arthritis Synovial Lesions

Abstract

Objective: To study the potential biomarkers and related pathways in rheumatoid arthritis (RA) synovial lesions, as well as immune cell, to provide theoretical basis and research directions for the mechanism and treatment of RA. Methods: Download the RA synovial tissue microarray data set (GSE77298, GSE55457 and GSE55235) from Gene Expression Omnibus (GEO), The“limma” package of R to identify differentially expressed genes (DEGs), DAVIA Perform GO (Gene Ontology, gene ontology) and KEGG (Kyoto Encyclopedia of Genes and Genomes, Kyoto Gene Encyclopedia) enrichment analysis. STRING (Search Tool for the Retrieval of Interacting Genes) constructs a Protein Protein Interaction Network (PPI), R screens Hub genes, and mines targeted miRNAs of Hub genes based on multiple databases. In R,the immune cell of RA synovial tissue samples are obtained through the three packages of "e1071", "parallel" and "preprocessCore" with "CIBERSORT" software. Results: Ten Hub genes (KIAA0101, FOXM1, EGFR, CDC20, BUB1B, TYMS, TOP2A, RRM2, JUN and CCNA2) and 2 key miRNAs (miR-520d-5p and miR) related to RA synovial lesions were finally identified -139-5p), significantly enriched in epithelial cell signaling, ECM-receptor interaction, estrogen signaling pathway, cell cycle, ErbB signaling pathway and GnRH signaling pathway in Helicobacter pylori infection. Immune cell analysis found that resting dendritic cells, B cells memory, dendritic cells activated, plasma cells, macrophages M1, mast cells resting and T cells regulatory have high expression in RA, while neutrophils, B cells naive and natural killer cells activated have low expression in RA. Conclusion:The Hub genes, key miRNAs, related pathways, and immune cell obtained in this study provide a certain basis for the etiology and treatment of RA synovial lesions.