title: Increased expression and secretion of resistin in epicardial adipose tissue of patients with acute coronary syndrome.
abstract: The purpose of this study was to test the hypothesis that specific epicardial adipose tissue (EAT) proinflammatory adipokines might be implicated in acute coronary syndrome (ACS). We compared expression and protein secretion of several EAT adipokines of male ACS with those of matched stable coronary artery disease (CAD) patients and controls with angiographically normal coronary arteries. The effect of supernatant of cultured EAT on endothelial cell permeability in vitro was also evaluated in the three study groups. EAT of ACS patients showed significantly higher gene expression and protein secretion of resistin than patients with stable CAD. Interleukin-6, plasminogen activator inhibitor-1, and monocyte chemoattractant protein-1 genes were also significantly overexpressed in ACS compared with the control group but not when compared with stable CAD. Immunofluorescence of EAT sections revealed a significantly greater number of CD68(+) cells in ACS patients than stable CAD and control groups. The permeability of endothelial cells in vitro was significantly increased after exposure to supernatant of cultured EAT from ACS, but not control or stable CAD groups, and this effect was normalized by anti-resistin antiserum. We found that EAT of patients with ACS is characterized by increased expression and secretion of resistin and associated with increased in vitro endothelial cell permeability.
authors.affiliation: San Raffaele Scientific Institute, Milan, Italy.
authors.forename: Silvia
authors.initials: S
authors.lastname: Langheim
authors.forename: Lorella
authors.initials: L
authors.lastname: Dreas
authors.forename: Lorenzo
authors.initials: L
authors.lastname: Veschini
authors.forename: Francesco
authors.initials: F
authors.lastname: Maisano
authors.forename: Chiara
authors.initials: C
authors.lastname: Foglieni
authors.forename: Santo
authors.initials: S
authors.lastname: Ferrarello
authors.forename: Gianfranco
authors.initials: G
authors.lastname: Sinagra
authors.forename: Bartolo
authors.initials: B
authors.lastname: Zingone
authors.forename: Ottavio
authors.initials: O
authors.lastname: Alfieri
authors.forename: Elisabetta
authors.initials: E
authors.lastname: Ferrero
authors.forename: Attilio
authors.initials: A
authors.lastname: Maseri
authors.forename: Giacomo
authors.initials: G
authors.lastname: Ruotolo
mesh_terms: D054058:Acute Coronary Syndrome / Q000378:metabolism* / Q000503:physiopathology / Q000601:surgery; D000273:Adipose Tissue / Q000378:metabolism* / Q000503:physiopathology; D000368:Aged; D016022:Case-Control Studies; D002465:Cell Movement / Q000502:physiology; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000378:metabolism; D001026:Coronary Artery Bypass; D003324:Coronary Artery Disease / Q000378:metabolism / Q000503:physiopathology; D003331:Coronary Vessels / Q000378:metabolism / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D015850:Interleukin-6 / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010496:Pericardium / Q000378:metabolism* / Q000503:physiopathology; D017395:Plasminogen Activator Inhibitor 1 / Q000378:metabolism; D052243:Resistin / Q000378:metabolism*
chemical_list: C111835:CCL2 protein, human; D018932:Chemokine CCL2; D015850:Interleukin-6; D017395:Plasminogen Activator Inhibitor 1; D052243:Resistin