Screening and Identification of Potential Hub Genes in Myocardial Infarction Through Bioinformatics Analysis.


Journal

Clinical interventions in aging
ISSN: 1178-1998
Titre abrégé: Clin Interv Aging
Pays: New Zealand
ID NLM: 101273480

Informations de publication

Date de publication:
2020
Historique:
received: 11 09 2020
accepted: 13 11 2020
entrez: 9 12 2020
pubmed: 10 12 2020
medline: 13 4 2021
Statut: epublish

Résumé

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. 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. 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. Expression levels of

Sections du résumé

BACKGROUND BACKGROUND
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 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 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 CONCLUSIONS
Expression levels of

Identifiants

pubmed: 33293800
doi: 10.2147/CIA.S281290
pii: 281290
pmc: PMC7718865
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

2233-2243

Informations de copyright

© 2020 Yu et al.

Déclaration de conflit d'intérêts

The authors report no conflicts of interest for this work.

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Auteurs

Yong-Wei Yu (YW)

Department of Cardiology, The Second Affiliated and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 312500, People's Republic of China.

Yang-Jing Xue (YJ)

Department of Cardiology, The Second Affiliated and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 312500, People's Republic of China.

La-La Qian (LL)

Department of Cardiology, Pingyang County Hospital of Traditional Chinese Medicine, Wenzhou 312500, People's Republic of China.

Zhi Chen (Z)

Department of Cardiology, Pingyang County Hospital of Traditional Chinese Medicine, Wenzhou 312500, People's Republic of China.

Jia-Qun Que (JQ)

Department of Cardiology, The Second Affiliated and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 312500, People's Republic of China.

Kai-Yu Huang (KY)

Department of Cardiology, The Second Affiliated and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 312500, People's Republic of China.

Shuai Liu (S)

Department of Cardiology, The Second Affiliated and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 312500, People's Republic of China.

Ying-Bei Weng (YB)

Department of Cardiology, The Second Affiliated and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 312500, People's Republic of China.

Fang-Ning Rong (FN)

Department of Cardiology, The Second Affiliated and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 312500, People's Republic of China.

Kang-Ting Ji (KT)

Department of Cardiology, The Second Affiliated and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 312500, People's Republic of China.

Jing-Ni Zeng (JN)

Department of Cardiology, The Second Affiliated and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 312500, People's Republic of China.

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