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Epicardial Adipose Tissue Has a Unique Transcriptome that is Modified in Severe Coronary Artery Disease
OBJECTIVE: To explore the transcriptome of epicardial adipose tissue (EAT) as compared to subcutaneous adipose tissue (SAT) and its modifications in a small number of patients with coronary artery disease (CAD) versus valvulopathy. DESIGN AND METHODS: SAT and EAT samples were obtained during electiv...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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2015
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5003780/ https://www.ncbi.nlm.nih.gov/pubmed/25959145 http://dx.doi.org/10.1002/oby.21059 |
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author | McAninch, Elizabeth A. Fonseca, Tatiana L. Poggioli, Raffaella Panos, Anthony L. Salerno, Tomas A. Deng, Youping Li, Yan Bianco, Antonio C. Iacobellis, Gianluca |
author_facet | McAninch, Elizabeth A. Fonseca, Tatiana L. Poggioli, Raffaella Panos, Anthony L. Salerno, Tomas A. Deng, Youping Li, Yan Bianco, Antonio C. Iacobellis, Gianluca |
author_sort | McAninch, Elizabeth A. |
collection | PubMed |
description | OBJECTIVE: To explore the transcriptome of epicardial adipose tissue (EAT) as compared to subcutaneous adipose tissue (SAT) and its modifications in a small number of patients with coronary artery disease (CAD) versus valvulopathy. DESIGN AND METHODS: SAT and EAT samples were obtained during elective cardiothoracic surgeries. The transcriptome of EAT was evaluated using an unbiased, whole-genome approach as compared to SAT in subjects with CAD (n=6) and without CAD (n=5), where the patients without CAD had cardiac valvulopathy. RESULTS: Relative to SAT, EAT is a highly inflammatory tissue enriched with genes involved in endothelial function, coagulation, immune signaling, potassium transport and apoptosis. EAT is lacking in expression of genes involved in protein metabolism, TGF-beta signaling, and oxidative stress. Although underpowered, in subjects with severe CAD, there is an expression trend suggesting widespread downregulation of EAT encompassing a diverse group of gene sets related to intracellular trafficking, proliferation/transcription regulation, protein catabolism, innate immunity/lectin pathway and ER stress. CONCLUSIONS: The EAT transcriptome is unique when compared to SAT. In the setting of CAD versus valvulopathy, there is possible alteration of the EAT transcriptome with gene suppression. This pilot study explores the transcriptome of EAT in CAD and valvulopathy, providing new insight into its physiologic and pathophysiologic roles. |
format | Online Article Text |
id | pubmed-5003780 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
record_format | MEDLINE/PubMed |
spelling | pubmed-50037802016-08-30 Epicardial Adipose Tissue Has a Unique Transcriptome that is Modified in Severe Coronary Artery Disease McAninch, Elizabeth A. Fonseca, Tatiana L. Poggioli, Raffaella Panos, Anthony L. Salerno, Tomas A. Deng, Youping Li, Yan Bianco, Antonio C. Iacobellis, Gianluca Obesity (Silver Spring) Article OBJECTIVE: To explore the transcriptome of epicardial adipose tissue (EAT) as compared to subcutaneous adipose tissue (SAT) and its modifications in a small number of patients with coronary artery disease (CAD) versus valvulopathy. DESIGN AND METHODS: SAT and EAT samples were obtained during elective cardiothoracic surgeries. The transcriptome of EAT was evaluated using an unbiased, whole-genome approach as compared to SAT in subjects with CAD (n=6) and without CAD (n=5), where the patients without CAD had cardiac valvulopathy. RESULTS: Relative to SAT, EAT is a highly inflammatory tissue enriched with genes involved in endothelial function, coagulation, immune signaling, potassium transport and apoptosis. EAT is lacking in expression of genes involved in protein metabolism, TGF-beta signaling, and oxidative stress. Although underpowered, in subjects with severe CAD, there is an expression trend suggesting widespread downregulation of EAT encompassing a diverse group of gene sets related to intracellular trafficking, proliferation/transcription regulation, protein catabolism, innate immunity/lectin pathway and ER stress. CONCLUSIONS: The EAT transcriptome is unique when compared to SAT. In the setting of CAD versus valvulopathy, there is possible alteration of the EAT transcriptome with gene suppression. This pilot study explores the transcriptome of EAT in CAD and valvulopathy, providing new insight into its physiologic and pathophysiologic roles. 2015-05-09 2015-06 /pmc/articles/PMC5003780/ /pubmed/25959145 http://dx.doi.org/10.1002/oby.21059 Text en http://www.nature.com/authors/editorial_policies/license.html#terms Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use:http://www.nature.com/authors/editorial_policies/license.html#terms |
spellingShingle | Article McAninch, Elizabeth A. Fonseca, Tatiana L. Poggioli, Raffaella Panos, Anthony L. Salerno, Tomas A. Deng, Youping Li, Yan Bianco, Antonio C. Iacobellis, Gianluca Epicardial Adipose Tissue Has a Unique Transcriptome that is Modified in Severe Coronary Artery Disease |
title | Epicardial Adipose Tissue Has a Unique Transcriptome that is Modified in Severe Coronary Artery Disease |
title_full | Epicardial Adipose Tissue Has a Unique Transcriptome that is Modified in Severe Coronary Artery Disease |
title_fullStr | Epicardial Adipose Tissue Has a Unique Transcriptome that is Modified in Severe Coronary Artery Disease |
title_full_unstemmed | Epicardial Adipose Tissue Has a Unique Transcriptome that is Modified in Severe Coronary Artery Disease |
title_short | Epicardial Adipose Tissue Has a Unique Transcriptome that is Modified in Severe Coronary Artery Disease |
title_sort | epicardial adipose tissue has a unique transcriptome that is modified in severe coronary artery disease |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5003780/ https://www.ncbi.nlm.nih.gov/pubmed/25959145 http://dx.doi.org/10.1002/oby.21059 |
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