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Weighted gene co-expression network analysis identifies specific modules and hub genes related to coronary artery disease

BACKGROUND: The analysis of the potential molecule targets of coronary artery disease (CAD) is critical for understanding the molecular mechanisms of disease. However, studies of global microarray gene co-expression analysis of CAD still remain limited. METHODS: Microarray data of CAD (GSE23561) wer...

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Autores principales: Liu, Jing, Jing, Ling, Tu, Xilin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4779223/
https://www.ncbi.nlm.nih.gov/pubmed/26944061
http://dx.doi.org/10.1186/s12872-016-0217-3
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author Liu, Jing
Jing, Ling
Tu, Xilin
author_facet Liu, Jing
Jing, Ling
Tu, Xilin
author_sort Liu, Jing
collection PubMed
description BACKGROUND: The analysis of the potential molecule targets of coronary artery disease (CAD) is critical for understanding the molecular mechanisms of disease. However, studies of global microarray gene co-expression analysis of CAD still remain limited. METHODS: Microarray data of CAD (GSE23561) were downloaded from Gene Expression Omnibus, including peripheral blood samples from CAD patients (n = 6) and controls (n = 9). Limma package in R was used to identify the differentially expressed genes (DEGs) between CAD and control samples. Using weighted gene co-expression network analysis (WGCNA) package in R, WGCNA was performed to identify significant modules in the network. Then, functional and pathway enrichment analyses were conducted for genes in the most significant module using DAVID software. Moreover, hub genes in the module were analyzed by isubpathwayminer package in R and GenCLiP 2.0 tool to identify the significant sub-pathways. RESULTS: Total 3711 DEGs and 21 modules for them were identified in CAD samples. The most significant module was associated with the pathways of hypertrophic cardiomyopathy and membrane related functions. In addition, the top 30 hub genes with high connectivity in the module were selected, and two genes (G6PD and S100A7) were taken as key molecules via sub-pathway screening and data mining. CONCLUSIONS: A module associated with hypertrophic cardiomyopathy pathway was detected in CAD samples. G6PD and S100A7 were the potential targets in CAD. Our finding might provide novel insight into the underlying molecular mechanism of CAD.
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spelling pubmed-47792232016-03-06 Weighted gene co-expression network analysis identifies specific modules and hub genes related to coronary artery disease Liu, Jing Jing, Ling Tu, Xilin BMC Cardiovasc Disord Research Article BACKGROUND: The analysis of the potential molecule targets of coronary artery disease (CAD) is critical for understanding the molecular mechanisms of disease. However, studies of global microarray gene co-expression analysis of CAD still remain limited. METHODS: Microarray data of CAD (GSE23561) were downloaded from Gene Expression Omnibus, including peripheral blood samples from CAD patients (n = 6) and controls (n = 9). Limma package in R was used to identify the differentially expressed genes (DEGs) between CAD and control samples. Using weighted gene co-expression network analysis (WGCNA) package in R, WGCNA was performed to identify significant modules in the network. Then, functional and pathway enrichment analyses were conducted for genes in the most significant module using DAVID software. Moreover, hub genes in the module were analyzed by isubpathwayminer package in R and GenCLiP 2.0 tool to identify the significant sub-pathways. RESULTS: Total 3711 DEGs and 21 modules for them were identified in CAD samples. The most significant module was associated with the pathways of hypertrophic cardiomyopathy and membrane related functions. In addition, the top 30 hub genes with high connectivity in the module were selected, and two genes (G6PD and S100A7) were taken as key molecules via sub-pathway screening and data mining. CONCLUSIONS: A module associated with hypertrophic cardiomyopathy pathway was detected in CAD samples. G6PD and S100A7 were the potential targets in CAD. Our finding might provide novel insight into the underlying molecular mechanism of CAD. BioMed Central 2016-03-05 /pmc/articles/PMC4779223/ /pubmed/26944061 http://dx.doi.org/10.1186/s12872-016-0217-3 Text en © Liu et al. 2016 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 Article
Liu, Jing
Jing, Ling
Tu, Xilin
Weighted gene co-expression network analysis identifies specific modules and hub genes related to coronary artery disease
title Weighted gene co-expression network analysis identifies specific modules and hub genes related to coronary artery disease
title_full Weighted gene co-expression network analysis identifies specific modules and hub genes related to coronary artery disease
title_fullStr Weighted gene co-expression network analysis identifies specific modules and hub genes related to coronary artery disease
title_full_unstemmed Weighted gene co-expression network analysis identifies specific modules and hub genes related to coronary artery disease
title_short Weighted gene co-expression network analysis identifies specific modules and hub genes related to coronary artery disease
title_sort weighted gene co-expression network analysis identifies specific modules and hub genes related to coronary artery disease
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4779223/
https://www.ncbi.nlm.nih.gov/pubmed/26944061
http://dx.doi.org/10.1186/s12872-016-0217-3
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