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Genomics of neonatal sepsis: has-miR-150 targeting BCL11B functions in disease progression

BACKGROUND: Neonatal sepsis is an inflammatory systemic syndrome, which is a major cause of morbidity and mortality in premature infants. We analyzed the expression profile data of E-MTAB-4785 to reveal the pathogenesis of the disease. METHODS: The expression profile dataset E-MTAB-4785, which conta...

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Autores principales: Huang, Li, Qiao, Lixing, Zhu, Huan, Jiang, Li, Yin, Liping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6267077/
https://www.ncbi.nlm.nih.gov/pubmed/30497506
http://dx.doi.org/10.1186/s13052-018-0575-9
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author Huang, Li
Qiao, Lixing
Zhu, Huan
Jiang, Li
Yin, Liping
author_facet Huang, Li
Qiao, Lixing
Zhu, Huan
Jiang, Li
Yin, Liping
author_sort Huang, Li
collection PubMed
description BACKGROUND: Neonatal sepsis is an inflammatory systemic syndrome, which is a major cause of morbidity and mortality in premature infants. We analyzed the expression profile data of E-MTAB-4785 to reveal the pathogenesis of the disease. METHODS: The expression profile dataset E-MTAB-4785, which contained 17 sepsis samples and 19 normal samples, was obtained from the ArrayExpress database. The differentially expressed genes (DEGs) were analyzed by the Bayesian testing method in limma package. Based on the DAVID online tool, enrichment analysis was conducted for the DEGs. Using STRING database and Cytoscape software, protein-protein interaction (PPI) network and module analyses were performed. Besides, transcription factor (TF)-DEG regulatory network was also constructed by Cytoscape software. Additionally, miRNA-DEG pairs were searched using miR2Disease and miRWalk 2.0 databases, followed by miRNA-DEG regulatory network was visualized by Cytoscape software. RESULTS: A total of 275 DEGs were identified from the sepsis samples in comparison to normal samples. TSPO, MAPK14, and ZAP70 were the hub nodes in the PPI network. Pathway enrichment analysis indicated that CEBPB and MAPK14 were enriched in TNF signaling pathway. Moreover, CEBPB and has-miR-150 might function in neonatal sepsis separately through targeting MAPK14 and BCL11B in the regulatory networks. These genes and miRNA might be novel targets for the clinical treatment of neonatal sepsis. CONCLUSION: TSPO, ZAP70, CEBPB targeting MAPK14, has-miR-150 targeting BCL11B might affect the pathogenesis of neonatal sepsis. However, their roles in neonatal sepsis still needed to be confirmed by further experimental researches.
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spelling pubmed-62670772018-12-05 Genomics of neonatal sepsis: has-miR-150 targeting BCL11B functions in disease progression Huang, Li Qiao, Lixing Zhu, Huan Jiang, Li Yin, Liping Ital J Pediatr Research BACKGROUND: Neonatal sepsis is an inflammatory systemic syndrome, which is a major cause of morbidity and mortality in premature infants. We analyzed the expression profile data of E-MTAB-4785 to reveal the pathogenesis of the disease. METHODS: The expression profile dataset E-MTAB-4785, which contained 17 sepsis samples and 19 normal samples, was obtained from the ArrayExpress database. The differentially expressed genes (DEGs) were analyzed by the Bayesian testing method in limma package. Based on the DAVID online tool, enrichment analysis was conducted for the DEGs. Using STRING database and Cytoscape software, protein-protein interaction (PPI) network and module analyses were performed. Besides, transcription factor (TF)-DEG regulatory network was also constructed by Cytoscape software. Additionally, miRNA-DEG pairs were searched using miR2Disease and miRWalk 2.0 databases, followed by miRNA-DEG regulatory network was visualized by Cytoscape software. RESULTS: A total of 275 DEGs were identified from the sepsis samples in comparison to normal samples. TSPO, MAPK14, and ZAP70 were the hub nodes in the PPI network. Pathway enrichment analysis indicated that CEBPB and MAPK14 were enriched in TNF signaling pathway. Moreover, CEBPB and has-miR-150 might function in neonatal sepsis separately through targeting MAPK14 and BCL11B in the regulatory networks. These genes and miRNA might be novel targets for the clinical treatment of neonatal sepsis. CONCLUSION: TSPO, ZAP70, CEBPB targeting MAPK14, has-miR-150 targeting BCL11B might affect the pathogenesis of neonatal sepsis. However, their roles in neonatal sepsis still needed to be confirmed by further experimental researches. BioMed Central 2018-11-29 /pmc/articles/PMC6267077/ /pubmed/30497506 http://dx.doi.org/10.1186/s13052-018-0575-9 Text en © The Author(s). 2018 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Huang, Li
Qiao, Lixing
Zhu, Huan
Jiang, Li
Yin, Liping
Genomics of neonatal sepsis: has-miR-150 targeting BCL11B functions in disease progression
title Genomics of neonatal sepsis: has-miR-150 targeting BCL11B functions in disease progression
title_full Genomics of neonatal sepsis: has-miR-150 targeting BCL11B functions in disease progression
title_fullStr Genomics of neonatal sepsis: has-miR-150 targeting BCL11B functions in disease progression
title_full_unstemmed Genomics of neonatal sepsis: has-miR-150 targeting BCL11B functions in disease progression
title_short Genomics of neonatal sepsis: has-miR-150 targeting BCL11B functions in disease progression
title_sort genomics of neonatal sepsis: has-mir-150 targeting bcl11b functions in disease progression
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6267077/
https://www.ncbi.nlm.nih.gov/pubmed/30497506
http://dx.doi.org/10.1186/s13052-018-0575-9
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