Identification of Potential Molecular Mechanisms and Candidate Genes Involved in The Acute Phase of Myocardial Infarction

Yushuang Yang; Jie Yang; Fenghua Sui; Pengfei Huo; Hailing Yang

doi:10.22074/cellj.2018.5213

Identification of Potential Molecular Mechanisms and Candidate Genes Involved in The Acute Phase of Myocardial Infarction

Cell J. 2018 Oct;20(3):435-442. doi: 10.22074/cellj.2018.5213. Epub 2018 May 15.

Authors

Yushuang Yang¹, Jie Yang¹, Fenghua Sui², Pengfei Huo³, Hailing Yang⁴

Affiliations

¹ Department of Endocrinology, China-Japan Union Hospital, Jilin University, Changchun, China.
² Cardiovascular Medicine, China-Japan Union Hospital (Xinmin District), Jilin University, Changchun, China.
³ Intensive Care Unit, China-Japan Union Hospital, Jilin University, Changchun, China. Electronic Address:suiyang1023@sina.com.
⁴ Department of Emergency, China-Japan Union Hospital, Jilin University, Changchun, China.

Abstract

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.

Keywords: Gene Expression Profile; Myocardial Infarction; Protein-Protein Interaction Network; Transcriptional Regulatory Network.