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Differential gene expression in human abdominal aortic aneurysm and aortic occlusive disease
Abdominal aortic aneurysm (AAA) and aortic occlusive disease (AOD) represent common causes of morbidity and mortality in elderly populations which were previously believed to have common aetiologies. The aim of this study was to assess the gene expression in human AAA and AOD. We performed microarra...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals LLC
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4536993/ https://www.ncbi.nlm.nih.gov/pubmed/25944698 |
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author | Biros, Erik Gäbel, Gabor Moran, Corey S. Schreurs, Charlotte Lindeman, Jan H. N. Walker, Philip J. Nataatmadja, Maria West, Malcolm Holdt, Lesca M. Hinterseher, Irene Pilarsky, Christian Golledge, Jonathan |
author_facet | Biros, Erik Gäbel, Gabor Moran, Corey S. Schreurs, Charlotte Lindeman, Jan H. N. Walker, Philip J. Nataatmadja, Maria West, Malcolm Holdt, Lesca M. Hinterseher, Irene Pilarsky, Christian Golledge, Jonathan |
author_sort | Biros, Erik |
collection | PubMed |
description | Abdominal aortic aneurysm (AAA) and aortic occlusive disease (AOD) represent common causes of morbidity and mortality in elderly populations which were previously believed to have common aetiologies. The aim of this study was to assess the gene expression in human AAA and AOD. We performed microarrays using aortic specimen obtained from 20 patients with small AAAs (≤ 55mm), 29 patients with large AAAs (> 55mm), 9 AOD patients, and 10 control aortic specimens obtained from organ donors. Some differentially expressed genes were validated by quantitative-PCR (qRT-PCR)/immunohistochemistry. We identified 840 and 1,014 differentially expressed genes in small and large AAAs, respectively. Immune-related pathways including cytokine-cytokine receptor interaction and T-cell-receptor signalling were upregulated in both small and large AAAs. Examples of validated genes included CTLA4 (2.01-fold upregulated in small AAA, P = 0.002), NKTR (2.37-and 2.66-fold upregulated in small and large AAA with P = 0.041 and P = 0.015, respectively), and CD8A (2.57-fold upregulated in large AAA, P = 0.004). 1,765 differentially expressed genes were identified in AOD. Pathways upregulated in AOD included metabolic and oxidative phosphorylation categories. The UCP2 gene was downregulated in AOD (3.73-fold downregulated, validated P = 0.017). In conclusion, the AAA and AOD transcriptomes were very different suggesting that AAA and AOD have distinct pathogenic mechanisms. |
format | Online Article Text |
id | pubmed-4536993 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Impact Journals LLC |
record_format | MEDLINE/PubMed |
spelling | pubmed-45369932015-08-26 Differential gene expression in human abdominal aortic aneurysm and aortic occlusive disease Biros, Erik Gäbel, Gabor Moran, Corey S. Schreurs, Charlotte Lindeman, Jan H. N. Walker, Philip J. Nataatmadja, Maria West, Malcolm Holdt, Lesca M. Hinterseher, Irene Pilarsky, Christian Golledge, Jonathan Oncotarget Research Paper: Pathology Abdominal aortic aneurysm (AAA) and aortic occlusive disease (AOD) represent common causes of morbidity and mortality in elderly populations which were previously believed to have common aetiologies. The aim of this study was to assess the gene expression in human AAA and AOD. We performed microarrays using aortic specimen obtained from 20 patients with small AAAs (≤ 55mm), 29 patients with large AAAs (> 55mm), 9 AOD patients, and 10 control aortic specimens obtained from organ donors. Some differentially expressed genes were validated by quantitative-PCR (qRT-PCR)/immunohistochemistry. We identified 840 and 1,014 differentially expressed genes in small and large AAAs, respectively. Immune-related pathways including cytokine-cytokine receptor interaction and T-cell-receptor signalling were upregulated in both small and large AAAs. Examples of validated genes included CTLA4 (2.01-fold upregulated in small AAA, P = 0.002), NKTR (2.37-and 2.66-fold upregulated in small and large AAA with P = 0.041 and P = 0.015, respectively), and CD8A (2.57-fold upregulated in large AAA, P = 0.004). 1,765 differentially expressed genes were identified in AOD. Pathways upregulated in AOD included metabolic and oxidative phosphorylation categories. The UCP2 gene was downregulated in AOD (3.73-fold downregulated, validated P = 0.017). In conclusion, the AAA and AOD transcriptomes were very different suggesting that AAA and AOD have distinct pathogenic mechanisms. Impact Journals LLC 2015-04-15 /pmc/articles/PMC4536993/ /pubmed/25944698 Text en Copyright: © 2015 Biros et al. http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Paper: Pathology Biros, Erik Gäbel, Gabor Moran, Corey S. Schreurs, Charlotte Lindeman, Jan H. N. Walker, Philip J. Nataatmadja, Maria West, Malcolm Holdt, Lesca M. Hinterseher, Irene Pilarsky, Christian Golledge, Jonathan Differential gene expression in human abdominal aortic aneurysm and aortic occlusive disease |
title | Differential gene expression in human abdominal aortic aneurysm and aortic occlusive disease |
title_full | Differential gene expression in human abdominal aortic aneurysm and aortic occlusive disease |
title_fullStr | Differential gene expression in human abdominal aortic aneurysm and aortic occlusive disease |
title_full_unstemmed | Differential gene expression in human abdominal aortic aneurysm and aortic occlusive disease |
title_short | Differential gene expression in human abdominal aortic aneurysm and aortic occlusive disease |
title_sort | differential gene expression in human abdominal aortic aneurysm and aortic occlusive disease |
topic | Research Paper: Pathology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4536993/ https://www.ncbi.nlm.nih.gov/pubmed/25944698 |
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