Comparison of gene expression profiles and related pathways in chronic thromboembolic pulmonary hypertension

Chronic thromboembolic pulmonary hypertension (CTEPH) is one of the main causes of severe pulmonary hypertension. However, despite treatment (pulmonary endarterectomy), in approximately 15–20% of patients, pulmonary vascular resistance and pulmonary arterial pressure continue to increase. To date, l...

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Main Authors: GU, SONG, SU, PIXIONG, YAN, JUN, ZHANG, XITAO, AN, XIANGGUANG, GAO, JIE, XIN, RUI, LIU, YAN
Format: Online
Language:English
Published: D.A. Spandidos 2014
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3896458/
id pubmed-3896458
recordtype oai_dc
spelling pubmed-38964582014-01-21 Comparison of gene expression profiles and related pathways in chronic thromboembolic pulmonary hypertension GU, SONG SU, PIXIONG YAN, JUN ZHANG, XITAO AN, XIANGGUANG GAO, JIE XIN, RUI LIU, YAN Articles Chronic thromboembolic pulmonary hypertension (CTEPH) is one of the main causes of severe pulmonary hypertension. However, despite treatment (pulmonary endarterectomy), in approximately 15–20% of patients, pulmonary vascular resistance and pulmonary arterial pressure continue to increase. To date, little is known about the changes that occur in gene expression in CTEPH. The identification of genes associated with CTEPH may provide insight into the pathogenesis of CTEPH and may aid in diagnosis and treatment. In this study, we analyzed the gene expresion profiles of pulmonary artery endothelial cells from 5 patients with CTEPH and 5 healthy controls using oligonucleotide microarrays. Bioinformatics analyses using the Gene Ontology (GO) and KEGG databases were carried out to identify the genes and pathways specifically associated with CTEPH. Signal transduction networks were established to identify the core genes regulating the progression of CTEPH. A number of genes were found to be differentially expressed in the pulmonary artery endothelial cells from patients with CTEPH. In total, 412 GO terms and 113 pathways were found to be associated with our list of genes. All differential gene interactions in the Signal-Net network were analyzed. JAK3, GNA15, MAPK13, ARRB2 and F2R were the most significantly altered. Bioinformatics analysis may help gather and analyze large amounts of data in microarrays by means of rigorous experimental planning, scientific statistical analysis and the collection of complete data. In this study, a novel differential gene expression pattern was constructed. However, further studies are required to identify novel targets for the diagnosis and treatment of CTEPH. D.A. Spandidos 2014-02 2013-12-10 /pmc/articles/PMC3896458/ /pubmed/24337368 http://dx.doi.org/10.3892/ijmm.2013.1582 Text en Copyright © 2014, Spandidos Publications http://creativecommons.org/licenses/by/3.0 This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author GU, SONG
SU, PIXIONG
YAN, JUN
ZHANG, XITAO
AN, XIANGGUANG
GAO, JIE
XIN, RUI
LIU, YAN
spellingShingle GU, SONG
SU, PIXIONG
YAN, JUN
ZHANG, XITAO
AN, XIANGGUANG
GAO, JIE
XIN, RUI
LIU, YAN
Comparison of gene expression profiles and related pathways in chronic thromboembolic pulmonary hypertension
author_facet GU, SONG
SU, PIXIONG
YAN, JUN
ZHANG, XITAO
AN, XIANGGUANG
GAO, JIE
XIN, RUI
LIU, YAN
author_sort GU, SONG
title Comparison of gene expression profiles and related pathways in chronic thromboembolic pulmonary hypertension
title_short Comparison of gene expression profiles and related pathways in chronic thromboembolic pulmonary hypertension
title_full Comparison of gene expression profiles and related pathways in chronic thromboembolic pulmonary hypertension
title_fullStr Comparison of gene expression profiles and related pathways in chronic thromboembolic pulmonary hypertension
title_full_unstemmed Comparison of gene expression profiles and related pathways in chronic thromboembolic pulmonary hypertension
title_sort comparison of gene expression profiles and related pathways in chronic thromboembolic pulmonary hypertension
description Chronic thromboembolic pulmonary hypertension (CTEPH) is one of the main causes of severe pulmonary hypertension. However, despite treatment (pulmonary endarterectomy), in approximately 15–20% of patients, pulmonary vascular resistance and pulmonary arterial pressure continue to increase. To date, little is known about the changes that occur in gene expression in CTEPH. The identification of genes associated with CTEPH may provide insight into the pathogenesis of CTEPH and may aid in diagnosis and treatment. In this study, we analyzed the gene expresion profiles of pulmonary artery endothelial cells from 5 patients with CTEPH and 5 healthy controls using oligonucleotide microarrays. Bioinformatics analyses using the Gene Ontology (GO) and KEGG databases were carried out to identify the genes and pathways specifically associated with CTEPH. Signal transduction networks were established to identify the core genes regulating the progression of CTEPH. A number of genes were found to be differentially expressed in the pulmonary artery endothelial cells from patients with CTEPH. In total, 412 GO terms and 113 pathways were found to be associated with our list of genes. All differential gene interactions in the Signal-Net network were analyzed. JAK3, GNA15, MAPK13, ARRB2 and F2R were the most significantly altered. Bioinformatics analysis may help gather and analyze large amounts of data in microarrays by means of rigorous experimental planning, scientific statistical analysis and the collection of complete data. In this study, a novel differential gene expression pattern was constructed. However, further studies are required to identify novel targets for the diagnosis and treatment of CTEPH.
publisher D.A. Spandidos
publishDate 2014
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3896458/
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