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pmid:26998004
Expression profile analysis based on DNA microarray for patients undergoing off-pump coronary artery bypass surgery.
Yunpeng Sun · Yongsheng Gao · Jingnan Sun · Xuguang Liu · Dashi Ma · Chunye Ma · Yong Wang
Experimental and therapeutic medicine · 2016 doi:10.3892/etm.2016.3003
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Experiment
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Complete file
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The aim of this study was to explore the effects of OPCAB on the basis of the associated molecular mechanisms. GSE12486 expression profiles downloaded from the Gene Expression Omnibus database (GEO) were analyzed to identify the differentially expressed genes (DEGs). Principal component analysis (PCA) was conducted based on the expression profiles of DEGs. Function and pathway enrichment of upregulated DEGs was performed, followed by protein-protein interaction (PPI) network construction. Gene Set Enrichment Analysis (GSEA) was used for miRNA enrichment analysis based on expression profiles and prediction of their association with the disease. Cytoscape was applied to construct miRNA regulatory networks of DEGs. In total 64 DEGs were identified, including 63 upregulated and 1 downregulated gene. The first principal component in the PCA analysis was able to distinguish between pre- and post-OPCAB samples. Upregulated DEGs mainly enriched 20 Gene Ontology terms, such as chemokine activity, and 5 pathways including the chemokine signaling pathway. The constructed PPI network contained 234 edges and 55 nodes, and 10 upregulated hub nodes, including FBJ murine osteosarcoma viral oncogene homolog (FOS), were screened. A total of 36 miRNAs, including MIR-224 and MIR-7, were screened by GSEA enrichment analysis. A miRNA regulatory network including 176 edges and 97 nodes was constructed, showing the regulatory relationships between miRNAs and DEGs. For example, early growth response 2 (EGR2) was regulated by 8 miRNAs including MIR-150, MIR-142-3P, MIR-367 and MIR-224. 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"Chemotaxis", "2.21E-12", "CCL3, IL6, CCL2, C5AR1, IL8, CXCL2, S100A9, CCL8, CCL4, PROK2, CXCR4, CCL3L1, CCL3L3, CYR61"], ["BP", "GO:0006954", "Inflammatory response", "3.29E-12", "NFKBIZ, IL6, CCL3, CCL2, IL8, S100A8, CXCL2, S100A9, CCL8, CCL4, S100A12, FOS, PROK2, CXCR4, CCL3L1, CCL3L3, SELE"], ["BP", "GO:0007626", "Locomotory behavior", "8.03E-11", "CCL3, IL6, CCL2, C5AR1, IL8, CXCL2, S100A9, NR4A2, CCL8, CCL4, PROK2, CXCR4, CCL3L1, CCL3L3, CYR61"], ["BP", "GO:0006952", "Defense response", "3.10E-10", "NFKBIZ, IL6, CCL3, CCL2, C5AR1, IL8, S100A8, CXCL2, S100A9, CCL8, CCL4, S100A12, CD83, PROK2, FOS, CXCR4, CCL3L1, CCL3L3, SELE"], ["BP", "GO:0009611", "Response to wounding", "3.11E-09", "NFKBIZ, IL6, CCL3, CCL2, IL8, S100A8, CXCL2, S100A9, CCL8, CCL4, S100A12, FOS, PROK2, CXCR4, CCL3L1, CCL3L3, SELE"], ["BP", "GO:0010033", "Response to organic substance", "3.51E-09", "EGR1, IL6, EGR2, CCL2, PTGS2, SOCS3, NR4A2, NR4A3, PMAIP1, JUNB, CD83, FOS, DUSP1, BTG2, JUN, SELE, MYC, CYR61"], ["BP", "GO:0045944", "Positive regulation of transcription from RNA polymerase II promoter", "3.39E-07", "EGR1, FOS, IL6, EGR2, JUN, CSRNP1, NR4A2, ABRA, NR4A3, MYC, KLF4, JUNB"], ["BP", "GO:0002237", "Response to molecule of bacterial origin", "1.55E-06", "FOS, IL6, CCL2, PTGS2, SOCS3, JUN, SELE"], ["MF", "GO:0008009", "Chemokine activity", "2.25E-08", "CCL3, CCL2, IL8, CCL3L1, CXCL2, CCL3L3, CCL8, CCL4"], ["MF", "GO:0042379", "Chemokine receptor binding", "3.34E-08", "CCL3, CCL2, IL8, CCL3L1, CXCL2, CCL3L3, CCL8, CCL4"], ["MF", "GO:0003700", "Transcription factor activity", "2.99E-06", "EGR1, MAFF, EGR3, EGR2, CEBPD, NR4A2, NR4A3, FOSB, JUNB, FOS, ATF3, JUN, CSRNP1, BHLHE40, MYC, KLF4"], ["MF", "GO:0005125", "Cytokine activity", "1.02E-05", "CCL3, IL6, CCL2, IL8, CCL3L1, CXCL2, CCL3L3, CCL8, CCL4"], ["MF", "GO:0043565", "Sequence-specific DNA binding", "1.84E-05", "EGR1, MAFF, FOS, ATF3, CEBPD, JUN, NR4A2, NR4A3, FOSB, MYC, KLF4, JUNB"], ["MF", "GO:0030528", "Transcription regulator 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