Résumé
Objective: This study used bioinformatics to determine genetic factors involved in progression of acute myocardial infarction [MI]
Materials and Methods: In this prospective study, gene expression profile GSE59867 was downloaded from the Gene Expression Omnibus database, which contained 46 normal samples obtained from stable coronary artery disease patients [n=46] who were without history of MI [control] and 390 samples from patients [n=111] who had evolving ST-segment elevation myocardial infarction [STEMI] as the MI group. These samples were divided into 4 groups based on time points. After identification of differentially expressed genes [DEGs], we conducted hierarchical clustering and functional enrichment analysis. Protein interaction and transcriptional regulation among DEGs were analysed
Results: We observed 8 clusters of DEGs that had a peak or a minimum at the t=1 time point according to gene expression levels. Upregulated DEGs showed significant enrichment in the biological process, single-organism cellular process, response to stimulus and stress, and osteoclast differentiation and lysosome. Downregulated DEGs enriched in the T-cell receptor signalling pathway and natural killer cell mediated cytotoxicity. We identified multiple genes, including signal transducer and activator of transcription 3 [STAT3]; LCK proto-oncogene, Src family tyrosine kinase [LCK]; and FYN proto-oncogene, Src family tyrosine kinase [FYN] from the protein-protein interaction [PPI] network and/or the transcriptional regulatory network
Conclusion: Cytokine-mediated inflammation, lysosome and osteoclast differentiation, and metabolism processes, as well as STAT3 may be involved in the acute phase of MI