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Yong-Wei Yu,1,* Yang-Jing Xue,1,* La-La Qian,2 Zhi Chen,2 Jia-Qun Que,1 Kai-Yu Huang,1 Shuai Liu,1 Ying-Bei Weng,1 Fang-Ning Rong,1 Kang-Ting Ji,1 Jing-Ni Zeng1 1Department of Cardiology, The Second Affiliated and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou 312500, People’s Republic of China; 2Department of Cardiology, Pingyang County Hospital of Traditional Chinese Medicine, Wenzhou 312500, People’s Republic of China*These authors contributed equally to this workCorrespondence: Kang-Ting Ji; Jing-Ni ZengDepartment of Cardiology, The Second Affiliated and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou 312500, People’s Republic of ChinaEmail jikt@wmu.edu.cn; zengjn6015@163.comBackground: Myocardial infarction (MI) is a common cause of death worldwide. It is characterized by coronary artery occlusion that causes ischemia and hypoxia of myocardial cells, leading to irreversible myocardial damage.Materials and Methods: To explore potential targets for treatment of MI, we reorganized and analyzed two microarray datasets (GSE4648 and GSE775). The GEO2R tool was used to screen for differentially expressed genes (DEGs) between infarcted and normal myocardium. We used the Database for Annotation, Visualization and Integrated Discovery (DAVID) to perform Gene Ontology functional annotation analysis (GO analysis) and the Kyoto Encyclopedia of Genes and Genomes for pathway enrichment analysis (KEGG analysis). We examined protein–protein interactions to characterize the relationship between differentially expressed genes, and we screened potential hub genes according to the degree of connection. PCR and Western blotting were used to identify the core genes.Results: At different times of infarction, a total of 35 genes showed upregulation at all times; however, none of the genes showed downregulation at all 3 times. Similarly, 10 hub genes with high degrees of connectivity were identified. In vivo and in vitro experiments suggested that expression levels of MMP-9 increased at various times after myocardial infarction and that expression increased in a variety of cells simultaneously.Conclusion: Expression levels of MMP-9 increase throughout the course of acute myocardial infarction, and this expression has both positive and negative sides. Further studies are needed to explore the role of MMP-9 in MI treatment. The potential values of Il6, Spp1, Ptgs2, Serpine1, Plaur, Cxcl5, Lgals3, Serpinb2, and Cd14 are also worth exploring.Keywords: myocardial infarction, MMP-9, GEO, microarray dataset, hub gene |
