Literature DB >> 30074154

Bioinformatics Analysis of Genes and Pathways of CD11b+/Ly6Cintermediate Macrophages after Renal Ischemia-Reperfusion Injury.

Dong Sun1, Xin Wan1, Bin-Bin Pan1, Qing Sun2, Xiao-Bing Ji1, Feng Zhang1, Hao Zhang1, Chang-Chun Cao3,4.   

Abstract

Renal ischemia-reperfusion injury (IRI) is a major cause of acute kidney injury (AKI), which could induce the poor prognosis. The purpose of this study was to characterize the molecular mechanism of the functional changes of CDllb+/Ly6Cintermediate macrophages after renal IRI. The gene expression profiles of CDllb+/Ly6Cintermcdiate macrophages of the sham surgery mice, and the mice 4 h, 24 h and 9 days after renal IRI were downloaded from the Gene Expression Omnibus database. Analysis of mRNA expression profiles was conducted to identify differentially expressed genes (DEGs), biological processes and pathways by the series test of cluster. Protein-protein interaction network was constructed and analysed to discover the key genes. A total of 6738 DEGs were identified and assigned to 20 model profiles. DEGs in profile 13 were one of the predominant expression profiles, which are involved in immune cell chemotaxis and proliferation. Signet analysis showed that Atp5al, Atp5o, Cox4i, Cdc42, Rac2 and Nhp2 were the key genes involved in oxidation-reduction, apoptosis, migration, M1-M2 differentiation, and proliferation of macrophages. RPS18 may be an appreciate reference gene as it was stable in macrophages. The identified DEGs and their enriched pathways investigate factors that may participate in the functional changes of CD 1lb+Ly6Cintermediate macrophages after renal IRI. Moreover, the vital gene Nhp2 may involve the polarization of macrophages, which may be a new target to affect the process of AKI.

Entities:  

Keywords:  differentially expressed genes; functional enrichment analysis; macrophage; protein-protein interaction; renal ischemia-reperfiision injury; series test of cluster

Mesh:

Substances:

Year:  2018        PMID: 30074154      PMCID: PMC7089064          DOI: 10.1007/s11596-018-1848-7

Source DB:  PubMed          Journal:  Curr Med Sci        ISSN: 2523-899X


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