Analysis of Differentially Expressed Genes in Coronary Artery Disease by Integrated Microarray Analysis

Abstract

Coronary artery disease (CAD) is a major cause of end-stage cardiac disease. Although profound efforts have been made to illuminate the pathogenesis, the molecular mechanisms of CAD remain to be analyzed. To identify the candidate genes in the advancement of CAD, microarray dataset GSE23766 was downloaded from the Gene Expression Omnibus database. The differentially expressed genes (DEGs) were identified, and pathway and gene ontology (GO) enrichment analyses were performed. The protein-protein interaction network was constructed and the module analysis was performed using the Biological General Repository for Interaction Datasets (BioGRID) and Cytoscape. Additionally, target genes-miRNA regulatory network and target genes-TF regulatory network were constructed and analyzed. There were 894 DEGs between male human CAD samples and female human CAD samples, including 456 up regulated genes and 438 down regulated genes. Pathway enrichment analyses revealed that DEGs (up and down regulated) were mostly enriched in the superpathway of steroid hormone biosynthesis, ABC transporters, oxidative ethanol degradation III and Complement and coagulation cascades. Similarly, geneontology enrichment analyses revealed that DEGs (up and down regulated) were mostly enriched in the forebrain neuron differentiation, filopodium membrane, platelet degranulation and blood microparticle. In the PPI network and modules (up and down regulated), MYC, NPM1, TRPC7, UBC, FN1, HEMK1, IFT74 and VHL were hub genes. In the target genes-miRNA regulatory network and target genes—TF regulatory network (up and down regulated), TAOK1, KHSRP, HSD17B11 and PAH were target genes. In conclusion, the pathway and GO ontology enriched by DEGs may reveal the molecular mechanism of CAD. Its hub and target genes, MYC, NPM1, TRPC7, UBC, FN1, HEMK1, IFT74, VHL, TAOK1, KHSRP, HSD17B11 and PAH were expected to be new targets for CAD. Our finding provided clues for exploring molecular mechanism and developing new prognostics, diagnostic and therapeutic strategies for CAD.

The Diverse Roles of TAO Kinases in Health and Diseases

“…There are other physiological processes or pathogeneses reported to be TAOK-associated, with mechanisms yet to be defined. In a differentially expressed microarray assay, TAOK1 was found to be highly expressed in patients with coronary artery disease [ 71 ]. A missense variant in the kinase domain of TAOK2 (pV244M) was reported in natural killer cell proliferative disorder [ 72 ].…”

Analysis of Differentially Expressed Genes in the Dentate Gyrus and Anterior Cingulate Cortex in a Mouse Model of Depression

“…In this study, we used the empirical Bayes t -test (eBayes) to identify UCMS-induced DEGs in the DG and ACC [ 32 ]. Among them, DEGs with a fold change > 1.5 (∣log 2 (fold change) | >0.585) and fold change > 1.2 (∣log 2 (fold change) | >0.263) in the DG and ACC were used for comparative studies, which were performed using the limma R package for data processing and analysis [ 32 ]. A heat map of common DEGs in both the DG and ACC was produced using the “pheatmap” package (version 1.0.10) of R [ 33 ].…”

“…Furthermore, module analysis was performed by using the PEWCC plugin (version 1.0) to explore the clustering modules, which included the hub genes in the vast PPI network (join parameter > 0.5, overlap threshold > 0.8) [ 37 ]. Finally, the ClueGO plugin (version 2.5.6) was used to analyze the biological functions of the clustering modules, and P < 0.05 was considered statistically significant [ 32 , 38 ].…”

Integrated analysis of DNA methylation profile of HLA-G gene and imaging in coronary heart disease: Pilot study

“…Since genome-wide association studies (GWASs) present several limitations in explaining the genotype-phenotype relationship, major efforts have been made to design an epigenetic map able to bridge the gap between genome and environment providing novel useful non-invasive biomarkers for CHD [3][4][5][6][7]. In the last years, advanced network-oriented analysis unveiled specific molecular pathways underlying CHD-related endophenotypes, mainly endothelial inflammation, providing novel insight in disease pathobiology [8][9][10][11][12]. Some authors emphasized the key role of DNA methylation in regulating the human leukocyte antigen-G (HLA-G) gene expression involved in inflammatory-related pathways underlying CHD onset [13,14].…”