Coronary disease is not associated with robust alterations in inflammatory gene expression in human epicardial fat
AuthorsFitzgibbons, Timothy P.
Tran, Khanh-Van T.
Nicoloro, Sarah M.
Tam, Stanley Kc
Czech, Michael P.
UMass Chan AffiliationsProgram in Molecular Medicine
Department of Medicine, Division of Cardiovascular Medicine
Cellular and Molecular Physiology
Nutritional and Metabolic Diseases
Pathological Conditions, Signs and Symptoms
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AbstractEpicardial 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.
JCI Insight. 2019 Oct 17;4(20). pii: 124859. doi: 10.1172/jci.insight.124859. Link to article on publisher's site
Permanent Link to this Itemhttp://hdl.handle.net/20.500.14038/41235
RightsCopyright: © 2019, Fitzgibbons et al. This is an open access article published under the terms of the Creative Commons Attribution 4.0 International License.
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.