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Circulating Transforming Growth Factor-β1, Lipoprotein(a) and Cellular Adhesion Molecules in Angiographically Assessed Coronary Artery Disease

  • Natasa Bogavac-Stanojevic , Srdjan Djurovic , Zorana Jelic-Ivanovic , Vesna Spasojevic- Kalimanovska and Dimitra Kalimanovska-Ostric
Published/Copyright: June 1, 2005
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Clinical Chemistry and Laboratory Medicine (CCLM)
From the journal Volume 41 Issue 7

Abstract

Transforming growth factor β1 (TGF-β1) is involved in different physiological and pathological processes, including atherogenesis. High plasma lipoprotein(a) (Lp(a)) concentration is an established independent risk factor that may interfere with the plasmin-mediated TGF-β1 activation. Both Lp(a) and TGF-β1 are thought to influence the expression of cellular adhesion molecules (CAMs), also involved in the process of atherogenesis. Whereas many studies confirmed the association between high plasma Lp(a) levels and coronary artery disease (CAD), conflicting results were obtained in different studies in which the changes of TGF-β1 and CAM concentrations in CAD patients were investigated. The aim of this case-control study was to explore the association of circulating TGF-β1, Lp(a) and CAMs (intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin) levels with the occurrence and severity of angiographically assessed coronary artery disease. Plasma TGF-β1, Lp(a), ICAM-1, VCAM-1 and E-selectin concentrations were measured in 100 patients with angiographically assessed CAD and 100 healthy blood donors matched according to age and gender. Lp(a) and TGF-β1 were significantly higher in patients than in healthy controls (p < 0.001 and p < 0.01, respectively), but no significant correlation between the TGF-β1 and Lp(a) values was found. The CAM concentrations obtained in CAD patients did not differ significantly as compared with the corresponding values in the controls. None of the measured parameters were influenced by the severity of CAD.

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Published Online: 2005-06-01
Published in Print: 2003-07-21

Copyright © 2003 by Walter de Gruyter GmbH & Co. KG

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