Study on the mechanism of lung ischemia-reperfusion injury based on bioinformatics

Abstract

Objective: lung ischemia-reperfusion injury has always been a research hotspot in the field of lung transplantation. The purpose of this study is tantamount to explore the molecular mechanism, key genes and related signal pathways of ischemia-reperfusion in lung transplantation through bioinformatics analysis. Methods: data numbered GSE172222 were downloaded from the Gene Expression Omnibus (GEO). The expression data of pulmonary micro vascular endothelial cells at 6 hours of cold ischemia and 6 hours of cold ischemia + 2 hours of reperfusion were obtained, and the differences were analyzed by gene ontology (GO), Kyoto gene and genome encyclopedia (KEGG) and disease ontology (DO). The protein interaction network of differential genes was constructed by the STRING database (https://www.string-db.org/) and visualized by Cytoscape Software (http://www.cytoscape.org/). Key genes were screened by cytoHubba plug-ins and key modules were screened by MCODE plug-ins. Gene set enrichment analysis (GSEA) was utilized to further understand the function of differential genes. Results: a total of 189 differential genes were generated. These differential genes were mainly enriched in myeloid cell differentiation. DNA binding transcriptional activator activity, and MAPK signal pathway. Six key modules were screened by MCODE plug-in, and five key genes of FOS,EGR1,JUNB,ATF3,CEBPB were screened based on NCC algorithm in cytoHubba. GSEA enrichment analysis showed that the expression of differential genes was up-regulated in osteoclast differentiation pathway and down-regulated in fatty acid degradation. Conclusion: in this study, differential genes and related pathways in pulmonary micro vascular endothelial cells were screened by bioinformatics to help understand the molecular mechanism of pulmonary ischemia-reperfusion injury and provide ideas for the prevention and treatment of pulmonary ischemia-reperfusion injury.