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Bioinformatics Analysis of Genes and Pathways of CD11b(+)/Ly6C(intermediate) Macrophages after Renal Ischemia-Reperfusion Injury

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+/Ly6C(intermediate) macrophages after renal IRI. The gene expression...

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Autores principales: Sun, Dong, Wan, Xin, Pan, Bin-bin, Sun, Qing, Ji, Xiao-bing, Zhang, Feng, Zhang, Hao, Cao, Chang-chun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Huazhong University of Science and Technology 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7089064/
https://www.ncbi.nlm.nih.gov/pubmed/30074154
http://dx.doi.org/10.1007/s11596-018-1848-7
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author Sun, Dong
Wan, Xin
Pan, Bin-bin
Sun, Qing
Ji, Xiao-bing
Zhang, Feng
Zhang, Hao
Cao, Chang-chun
author_facet Sun, Dong
Wan, Xin
Pan, Bin-bin
Sun, Qing
Ji, Xiao-bing
Zhang, Feng
Zhang, Hao
Cao, Chang-chun
author_sort Sun, Dong
collection PubMed
description 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+/Ly6C(intermediate) 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(+)Ly6C(intermediate) 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
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spelling pubmed-70890642020-03-23 Bioinformatics Analysis of Genes and Pathways of CD11b(+)/Ly6C(intermediate) Macrophages after Renal Ischemia-Reperfusion Injury Sun, Dong Wan, Xin Pan, Bin-bin Sun, Qing Ji, Xiao-bing Zhang, Feng Zhang, Hao Cao, Chang-chun Curr Med Sci Article 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+/Ly6C(intermediate) 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(+)Ly6C(intermediate) 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 Huazhong University of Science and Technology 2018-03-15 2018 /pmc/articles/PMC7089064/ /pubmed/30074154 http://dx.doi.org/10.1007/s11596-018-1848-7 Text en © Huazhong University of Science and Technology 2018 This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.
spellingShingle Article
Sun, Dong
Wan, Xin
Pan, Bin-bin
Sun, Qing
Ji, Xiao-bing
Zhang, Feng
Zhang, Hao
Cao, Chang-chun
Bioinformatics Analysis of Genes and Pathways of CD11b(+)/Ly6C(intermediate) Macrophages after Renal Ischemia-Reperfusion Injury
title Bioinformatics Analysis of Genes and Pathways of CD11b(+)/Ly6C(intermediate) Macrophages after Renal Ischemia-Reperfusion Injury
title_full Bioinformatics Analysis of Genes and Pathways of CD11b(+)/Ly6C(intermediate) Macrophages after Renal Ischemia-Reperfusion Injury
title_fullStr Bioinformatics Analysis of Genes and Pathways of CD11b(+)/Ly6C(intermediate) Macrophages after Renal Ischemia-Reperfusion Injury
title_full_unstemmed Bioinformatics Analysis of Genes and Pathways of CD11b(+)/Ly6C(intermediate) Macrophages after Renal Ischemia-Reperfusion Injury
title_short Bioinformatics Analysis of Genes and Pathways of CD11b(+)/Ly6C(intermediate) Macrophages after Renal Ischemia-Reperfusion Injury
title_sort bioinformatics analysis of genes and pathways of cd11b(+)/ly6c(intermediate) macrophages after renal ischemia-reperfusion injury
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7089064/
https://www.ncbi.nlm.nih.gov/pubmed/30074154
http://dx.doi.org/10.1007/s11596-018-1848-7
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