info:eu-repo/semantics/article
Metalloproteinase 2 and 9 Activity Increase in Epicardial Adipose Tissue of Patients with Coronary Artery Disease
Fecha
2017-01Registro en:
Miksztowicz, Verónica Julieta; Morales, Celina; Barchuk, Magalí; López, Graciela; Póveda, Ricardo; et al.; Metalloproteinase 2 and 9 Activity Increase in Epicardial Adipose Tissue of Patients with Coronary Artery Disease; Bentham Science Publishers; Current Vascular Pharmacology; 15; 2; 1-2017; 135-143
1570-1611
CONICET Digital
CONICET
Autor
Miksztowicz, Verónica Julieta
Morales, Celina
Barchuk, Magalí
López, Graciela
Póveda, Ricardo
Gelpi, Ricardo Jorge
Schreier, Laura Ester
Rubio, Miguel
Berg, Gabriela Alicia
Resumen
Background: Epicardial adipose tissue (EAT) is a visceral adipose tissue (AT) surrounding and infiltrating myocardium and coronary arteries. Increased EAT may represent a chronic inflammatory injury and a link with coronary artery disease (CAD). Metalloproteinases (MMPs) are involved in expansion of AT. Objective: To evaluate MMP-2 and -9 behaviour in EAT from CAD patients. Methods: In EAT and subcutaneous AT (SAT) from patients undergoing coronary artery bypass graft (CABG, n=26) or valve replacement (No CABG, n=18), MMP-2 and -9 activity and localization, inflammatory cells and vascular endothelial growth factor (VEGF) levels were determined. Results: In EAT from CABG, MMP-2 and -9 activity was increased compared with No CABG (p=0.041 and p=0.027, respectively) and compared with SAT (p=0.005 and p=0.048, respectively). In CABG patients EAT showed higher infiltration of macrophages and T lymphocytes than SAT (p=0.01 and p=0.002, respectively). In No CABG patients no sign of cellular retention was observed in EAT or SAT. Vascular density was higher in EAT from CABG than No CABG (p=0.015) and it was directly correlated with MMP-2 (p=0.006) and MMP-9 (p=0.02). VEGF levels in EAT were directly associated with MMP-2 (p=0.016). Conclusion: In EAT from CABG patients the increase of MMP-2 and -9 activity and the presence of inflammatory cells would be partially responsible for extracellular matrix (ECM) remodeling and major vascular density necessary for EAT expansion. Improved knowledge of EAT behaviour may allow to identify new therapeutic targets for the treatment of CAD.