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.

Glucose uptake and lipid metabolism are impaired in epicardial adipose tissue from heart failure patients with or without diabetes

“…However, other studies have reported IL8 increases in EAT (70,88), perhaps due to population differences. Previous studies have reported that SERPINE1 was found to be increased in EAT from patients with severe stable CAD (70) and overexpressed in EAT from acute coronary syndrome (43). In our study, SERPINE1 gene expression correlates with the lipolysis results, indicating that increased lipolysis associates with increased inflammation observed in SAT, whereas the decreased lipolysis and inflammatory gene expression observed in EAT may indicate a possible protective mechanism toward the cardiomyocyte.…”

“…In our study, SERPINE1 gene expression correlates with the lipolysis results, indicating that increased lipolysis associates with increased inflammation observed in SAT, whereas the decreased lipolysis and inflammatory gene expression observed in EAT may indicate a possible protective mechanism toward the cardiomyocyte. Moreover, depending on the models studied, SERPINE1 may be regulated by insulin and by prescribed medications (25,43,53,76). However, we did not detect any effect of diabetes on inflammatory markers when comparing with nondiabetics with HF.…”

Roles of human epicardial adipose tissue in coronary artery atherosclerosis

“…Epicardial adipose tissue is a true visceral fat tissue that deposits not only on the free wall of right ventricle and on the left ventricular apex, but also around the atria [16,17] . The epicardial adipose tissue is significantly associated with the development of heart diseases [18][19][20] .…”

Effect Imbalance Aqueous Body Fluids, and Renal Dysfunction, Cardiovascular Survival in Patients After an Acute Coronary Syndrome, Myocardial Revascularization

“…Среди изученных посредников развития и прогрес-сирования эндотелиальной дисфункции необходи-мо отметить резистин, изучение которого в послед-нее время проводится не только в группе больных с метаболическим синдромом и сахарным диабетом, но и в когорте пациентов с ОКС. В 2010 году, на-учно-исследовательской группой показано, что при наличии острой ишемии миокарда концентрация плазменного резистина повышается, а вместе с тем увеличивается и проницаемость сосудов [13], что является одним из главных механизмов перераспре-деления водных секторов организма. Аналогичные данные были получены и при проведении других исследований по установлению зависимости кон-центрации резистина плазмы и прогрессирования атеросклероза [11].…”