Coronary disease is not associated with robust alterations in inflammatory gene expression in human epicardial fat
Authors
Fitzgibbons, Timothy P.Lee, Nancy
Tran, Khanh-Van T.
Nicoloro, Sarah M.
Kelly, Mark
Tam, Stanley Kc
Czech, Michael P.
UMass Chan Affiliations
Program in Molecular MedicineDepartment of Medicine, Division of Cardiovascular Medicine
Document Type
Journal ArticlePublication Date
2019-10-17Keywords
Adipose tissueAtherosclerosis
Cardiology
Inflammation
Obesity
Cardiology
Cardiovascular Diseases
Cellular and Molecular Physiology
Medical Physiology
Nutritional and Metabolic Diseases
Pathological Conditions, Signs and Symptoms
Physiological Processes
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Show full item recordAbstract
Epicardial adipose tissue (EAT) is the visceral fat depot of the heart. Inflammation of EAT is thought to contribute to coronary artery disease (CAD). Therefore, we hypothesized that the EAT of patients with CAD would have increased inflammatory gene expression compared with controls without CAD. Cardiac surgery patients with (n = 13) or without CAD (n = 13) were consented, and samples of EAT and subcutaneous adipose tissue (SAT) were obtained. Transcriptomic analysis was performed using Affymetrix Human Gene 1.0 ST arrays. Differential expression was defined as a 1.5-fold change (ANOVA P < 0.05). Six hundred ninety-three genes were differentially expressed between SAT and EAT in controls and 805 in cases. Expression of 326 genes was different between EAT of cases and controls; expression of 14 genes was increased in cases, while 312 were increased in controls. Quantitative reverse transcription PCR confirmed that there was no difference in expression of CCL2, CCR2, TNF-alpha, IL-6, IL-8, and PAI1 between groups. Immunohistochemistry showed more macrophages in EAT than SAT, but there was no difference in their number or activation state between groups. In contrast to prior studies, we did not find increased inflammatory gene expression in the EAT of patients with CAD. We conclude that the specific adipose tissue depot, rather than CAD status, is responsible for the majority of differential gene expression.Source
JCI Insight. 2019 Oct 17;4(20). pii: 124859. doi: 10.1172/jci.insight.124859. Link to article on publisher's site
DOI
10.1172/jci.insight.124859Permanent Link to this Item
http://hdl.handle.net/20.500.14038/41235PubMed ID
31513547Related Resources
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Copyright: © 2019, Fitzgibbons et al. This is an open access article published under the terms of the Creative Commons Attribution 4.0 International License.Distribution License
http://creativecommons.org/licenses/by/4.0/ae974a485f413a2113503eed53cd6c53
10.1172/jci.insight.124859
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Except where otherwise noted, this item's license is described as Copyright: © 2019, Fitzgibbons et al. This is an open access article published under the terms of the Creative Commons Attribution 4.0 International License.