title: Epicardial adipose tissue has a unique transcriptome modified in severe coronary artery disease.
abstract: 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.
  
  
  METHODS
  SAT and EAT samples were obtained during elective cardiothoracic surgeries. The transcriptome of EAT was evaluated, as compared to SAT, using an unbiased, whole-genome approach 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, tranforming growth factor-beta (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.
authors.affiliation: Department of Medicine, Division of Endocrinology and Metabolism, Rush University Medical Center, Chicago, Illinois, USA.
authors.forename: Elizabeth A
authors.initials: EA
authors.lastname: McAninch
authors.affiliation: Department of Medicine, Division of Endocrinology and Metabolism, Rush University Medical Center, Chicago, Illinois, USA.
authors.forename: Tatiana L
authors.initials: TL
authors.lastname: Fonseca
authors.affiliation: Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Miami Miller School of Medicine, Miami, Florida, USA.
authors.forename: Raffaella
authors.initials: R
authors.lastname: Poggioli
authors.affiliation: Department of Surgery, Division of Thoracic and Cardiac Surgery, University of Miami Miller School of Medicine, Miami, Florida, USA.
authors.forename: Anthony L
authors.initials: AL
authors.lastname: Panos
authors.affiliation: Department of Surgery, Division of Thoracic and Cardiac Surgery, University of Miami Miller School of Medicine, Miami, Florida, USA.
authors.forename: Tomas A
authors.initials: TA
authors.lastname: Salerno
authors.affiliation: Department of Medicine, Rush University Medical Center, Chicago, Illinois, USA.
authors.forename: Youping
authors.initials: Y
authors.lastname: Deng
authors.affiliation: Department of Medicine, Rush University Medical Center, Chicago, Illinois, USA.
authors.forename: Yan
authors.initials: Y
authors.lastname: Li
authors.affiliation: Department of Medicine, Division of Endocrinology and Metabolism, Rush University Medical Center, Chicago, Illinois, USA.
authors.forename: Antonio C
authors.initials: AC
authors.lastname: Bianco
authors.affiliation: Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Miami Miller School of Medicine, Miami, Florida, USA.
authors.forename: Gianluca
authors.initials: G
authors.lastname: Iacobellis
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism*; D003324:Coronary Artery Disease / Q000235:genetics / Q000378:metabolism*; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D008297:Male; D010496:Pericardium / Q000378:metabolism*; D010865:Pilot Projects; D059467:Transcriptome