Document Detail

Increased expression and secretion of resistin in epicardial adipose tissue of patients with acute coronary syndrome.
MedLine Citation:
PMID:  20061546     Owner:  NLM     Status:  MEDLINE    
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.
Silvia Langheim; Lorella Dreas; Lorenzo Veschini; Francesco Maisano; Chiara Foglieni; Santo Ferrarello; Gianfranco Sinagra; Bartolo Zingone; Ottavio Alfieri; Elisabetta Ferrero; Attilio Maseri; Giacomo Ruotolo
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-01-08
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  298     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2010 Mar 
Date Detail:
Created Date:  2010-02-25     Completed Date:  2010-04-02     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H746-53     Citation Subset:  IM    
San Raffaele Scientific Institute, Milan, Italy.
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MeSH Terms
Acute Coronary Syndrome / metabolism*,  physiopathology,  surgery
Adipose Tissue / metabolism*,  physiopathology
Case-Control Studies
Cell Movement / physiology
Cells, Cultured
Chemokine CCL2 / metabolism
Coronary Artery Bypass
Coronary Artery Disease / metabolism,  physiopathology
Coronary Vessels / metabolism,  physiopathology
Endothelium, Vascular / metabolism,  physiopathology
Interleukin-6 / metabolism
Middle Aged
Pericardium / metabolism*,  physiopathology
Plasminogen Activator Inhibitor 1 / metabolism
Resistin / metabolism*
Reg. No./Substance:
0/CCL2 protein, human; 0/Chemokine CCL2; 0/Interleukin-6; 0/Plasminogen Activator Inhibitor 1; 0/Resistin
Comment In:
Am J Physiol Heart Circ Physiol. 2010 Mar;298(3):H734-5   [PMID:  20097767 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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