Current Issue

Volume 20, Number 3, Autumn 2018, Serial Number: 79 Pages: 435-442

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


Yushuang Yang, B.Sc, 1, Jie Yang, Ph.D, 2, Fenghua Sui, B.Sc, 3, Pengfei Huo, M.M, 4, *, Hailing Yang, M.M, 5, *,
Department of Cardiovascular, China-Japan Union Hospital, Jilin University, Changchun, China
Department of Endocrinology, China-Japan Union Hospital, Jilin University, Changchun, China
Cardiovascular Medicine, China-Japan Union Hospital (Xinmin District), Jilin University, Changchun, China
Intensive Care Unit, China-Japan Union Hospital, Jilin University, Changchun, China
Department of Emergency, China-Japan Union Hospital, Jilin University, Changchun, China
*Corresponding Addresses: Intensive Care Unit China-Japan Union Hospital Jilin University No. 126 Xiantai Street Changchun 130031 China Department of Emergency China-Japan Union Hospital Jilin University Changchun China Emails:suiyang1023@sina.com,cczryhl@163.com

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.