Analysis of the molecular mechanisms of ulcerative colitis and atherosclerosis by microarray data

Adults can develop ulcerative colitis (UC), a chronic inflammatory illness of the colon, while atherosclerosis (AA) is a chronic inflammatory disease of the blood vessels caused by a range of risk factors. Prior research has demonstrated that UC increases the risk of AA, although the underlying pathological mechanisms are not entirely understood. The purpose of this work was to discover differentially expressed genes (DEGs) in UC and AA and investigate their molecular processes using a bioinformatics method. The UC (GSE36807) and AA (GSE28829) datasets were obtained from the Gene Expression Omnibus (GEO) database. Following the identification of genes that are differentially expressed in common with UC and AA, functional annotation, the construction of protein-protein interaction (PPI) networks and modules, the identification of hub genes, and co-expression analysis were carried out. A total of 105 (including 92 up-regulated and 13 down-regulated genes) DEGs were selected for correlation analysis in the above two datasets, and after Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional analysis immune responses, cytokines, and chemokines were found to play crucial roles in both diseases. Finally, a total of 16 hub genes were identified by CytoHubba and MCODE plugins in Cytoscape, including Chemokine (C-C motif) ligand 4(CCL4), Toll-like receptor 2 (TLR2), Integrin Beta 2(ITGB2), Chemokine (C-C motif) Receptor 1(CCR1), Toll-Like Receptor 8 (TLR8), Fc Fragment of IgG Receptor IIa (FCGR2A), Neutrophil Cytosolic Factor 2(NCF2), Leukocyte immunoglobulin-like receptor B2(LILRB2), FGR proto-oncogene, Src family tyrosine kinase(FGR), Intercellular Adhesion Molecule 1 (ICAM1), Caspase 1(CASP1), Matrix Metallopeptidase 9(MMP9), Cluster of Differentiation 163(CD163), Complement Component 5a Receptor 1 (C5AR1), Neutrophil Cytosolic Factor 4 (NCF4), Selectin P (SELP). This study discovered a link between UC and AA, as well as shared hub genes and pathways, which may bring new insights into the processes of UC and AA.