BACKGROUND: We aimed to predict key genes associated with acute myocardial infarction (AMI) by bioinformatics analysis. METHODS: The microarray data of GSE48060, including peripheral blood samples from 31 first-time AMI patients within 48-h post-MI and 21 normal controls, were obtained from Gene Expression Omnibus database. The differentially expressed genes (DEGs) in AMI samples compared with normal controls were identified. Functional enrichment analysis was then performed, followed by analysis of protein-protein interaction (PPI) network and transcription regulatory network (TRN). RESULTS: A total of 385 up- and 504 down-regulated DEGs were identified. They were mainly enriched in five pathways, such as natural killer (NK) cell-mediated cytotoxicity and chemokine signaling pathway. Chemokine (C-C motif) ligand 5 (CCL5) was hub protein in PPI network. Besides, four transcription factors (TFs), including nuclear receptor subfamily 2, group C, member 2 (NR2C2), MYC-associated factor X (MAX), general transcription factor IIIC, polypeptide 2, beta 110 kDa (GTF3C2), and B-cell CLL/lymphoma 3 (BCL3), were identified. Notably, nuclear receptor coactivator 7 (NCOA7) interacted with GTF3C2 and MAX directly. CONCLUSIONS: CCL5, BCL3, NR2C2, MAX, GTF3C2, and NCOA7 might play important roles in AMI development.
BACKGROUND: We aimed to predict key genes associated with acute myocardial infarction (AMI) by bioinformatics analysis. METHODS: The microarray data of GSE48060, including peripheral blood samples from 31 first-time AMI patients within 48-h post-MI and 21 normal controls, were obtained from Gene Expression Omnibus database. The differentially expressed genes (DEGs) in AMI samples compared with normal controls were identified. Functional enrichment analysis was then performed, followed by analysis of protein-protein interaction (PPI) network and transcription regulatory network (TRN). RESULTS: A total of 385 up- and 504 down-regulated DEGs were identified. They were mainly enriched in five pathways, such as natural killer (NK) cell-mediated cytotoxicity and chemokine signaling pathway. Chemokine (C-C motif) ligand 5 (CCL5) was hub protein in PPI network. Besides, four transcription factors (TFs), including nuclear receptor subfamily 2, group C, member 2 (NR2C2), MYC-associated factor X (MAX), general transcription factor IIIC, polypeptide 2, beta 110 kDa (GTF3C2), and B-cell CLL/lymphoma 3 (BCL3), were identified. Notably, nuclear receptor coactivator 7 (NCOA7) interacted with GTF3C2 and MAX directly. CONCLUSIONS:CCL5, BCL3, NR2C2, MAX, GTF3C2, and NCOA7 might play important roles in AMI development.