Abstract
BackgroundThe current research aimed to expound the genes and pathways that are involved in coronary artery disease (CAD) and ischaemic stroke (IS) and the related mechanisms.MethodsTwo array CAD datasets of (GSE66360 and GSE97320) and an array IS dataset (GSE22255) were downloaded. Differentially expressed genes (DEGs) were identified using the limma package. The online tool Database for Annotation, Visualization and Integrated Discovery (DAVID) (version 6.8; david.abcc.ncifcrf.gov) was used to annotate the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway and Gene Ontology (GO) enrichment analyses of the DEGs. A protein-protein interaction (PPI) network was constructed by Cytoscape software, and then Molecular Complex Detection (MCODE) analysis was used to screen for hub genes. The hub genes were also confirmed by RT-qPCR and unconditional logistic regression analysis in our CAD and IS patients.ResultsA total of 20 common DEGs (all upregulated) were identified between the CAD/IS and control groups. Eleven molecular functions, 3 cellular components, and 49 biological processes were confirmed by GO enrichment analysis, and the 20 common upregulated DEGs were enriched in 21 KEGG pathways. A PPI network including 24 nodes and 68 edges was constructed with the STRING online tool. After MCODE analysis, the top 5 high degree genes, including Jun proto-oncogene (JUN, degree = 9), C-X-C motif chemokine ligand 8 (CXCL8, degree = 9), tumour necrosis factor (TNF, degree = 9), suppressor of cytokine signalling 3 (SOCS3, degree = 8) and TNF alpha induced protein 3 (TNFAIP3, degree = 8) were noted. RT-qPCR results demonstrated that the expression levels of CXCL8 were increased in IS patients than in normal participants and the expression levels of SOCS3, TNF and TNFAIP were higher in CAD/IS patients than in normal participants. Meanwhile, unconditional logistic regression analysis revealed that the incidence of CAD or IS was positively correlated with the CXCL8, SOCS3, TNF and TNFAIP3.ConclusionsThe CXCL8, TNF, SOCS3 and TNFAIP3 associated with inflammation may serve as biomarkers for the diagnosis of CAD or IS. The possible mechanisms may involve the Toll-like receptor, TNF, NF-kappa B, cytokine-cytokine receptor interactions and the NOD-like receptor signalling pathways.
Highlights
The current research aimed to expound the genes and pathways that are involved in coronary artery disease (CAD) and ischaemic stroke (IS) and the related mechanisms
3 cellular components, and 49 biological processes were confirmed by Gene Ontology (GO) enrichment analysis, and the common upregulated Differentially expressed genes (DEGs) were enriched in Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways
RT-qPCR results demonstrated that the expression levels of C-X-C motif chemokine ligand 8 (CXCL8) were increased in IS patients than in normal participants and the expression levels of SOCS3, Tumor necrosis factor (TNF) and TNFAIP were higher in CAD/IS patients than in normal participants
Summary
The current research aimed to expound the genes and pathways that are involved in coronary artery disease (CAD) and ischaemic stroke (IS) and the related mechanisms. Coronary artery disease (CAD) and ischaemic stroke (IS) are prominent causes of disability, mortality, morbidity, functional deterioration and healthcare expenses and account for approximately 30% of all deaths worldwide [1,2,3,4]. There is some evidence of several shared genetic characteristics of both diseases [10] Both diseases are risk factors for one another [11, 12], and they are considered to be therapeutic targets for clinical research and for evaluating the risk of major adverse cardiac events (MACEs). There is a consensus on the effectiveness of the early prevention of CAD and IS
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