Life SciencesCardiologyMolecular BiologyGene ExpressionGenomicsInflammationCoronary Artery DiseaseDifferential Expression AnalysisDifferential Gene Expression AnalysisGene Expression ProfilingInflammatory SignalingTranscriptomic ProfilingDifferential Gene ExpressionDifferential Transcript ExpressionQuantitative Polymerase Chain ReactionReal-time Polymerase Chain Reaction (Pcr)Real-time Polymerase Chain Reaction AssaysRna SequencingRna Sequencing (Rna-seq)Rna Sequencing Differential Expression Analysis
BACKGROUND: Coronary artery disease (CAD) is a chronic inflammatory disease caused by development of atherosclerosis (AS), which is the leading cause of mortality and disability. Our study aimed to identify the differentially expressed genes (DEGs) in CD14+ monocytes from CAD patients compared with those from non-CAD controls, which might pave the way to diagnosis and treatment for CAD. METHODS: The RNA-sequencing (RNA-seq) was performed by BGISEQ-500, followed by analyzing with R package to screening DEGs. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed by R package. In addition, we validated the results of RNA-seq using real-time quantitative polymerase chain reaction (RT-qPCR). Furthermore, we explored the function of selected ten genes in LDL-treated CD14+ monocytes by RT-qPCR. RESULTS: a total of 2897 DEGs were identified, including 753 up- and 2144 down-regulated genes in CD14+ monocytes from CAD patients. These DEGs were mainly enriched in plasma membrane and cell periphery of cell component, immune system process of biological process, NF-κB signaling pathway, cell adhesion molecules signaling pathway and cytokine-cytokine receptor interaction signaling pathway. In LDL-treated CD14+ monocytes, the mRNA expression of pyruvate dehydrogenase kinase 4 (PDK4) was significantly up-regulated. CONCLUSION: In the present study, we suggested that PDK4 might play a role in progression of CAD. The study will provide some pieces of evidence to investigate the role and mechanism of key genes in the pathogenesis of CAD.
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