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Simvastatin and atorvastatin attenuate VCAM-1 and uPAR expression on human endothelial cells and platelet surface expression of CD40 ligand
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Abstract
Methods and Results: After a 24 h incubation period with either simvastatin or atorvastatin (1 μmol/L), human umbilical vein endothelial cells were stimulated for 1 h with lipopolysaccharide (LPS), and were then incubated in direct contact with activated platelets. Platelet surface expression of CD40L and CD62P and expression of ICAM-1, VCAM-1, uPAR and MT1-MMP on endothelial cells were measured by flow cytometry. Supernatants were analyzed by ELISA for soluble MMP-1. The increased expression of VCAM-1 and uPAR on endothelial cells by stimulation with LPS and by direct contact with activated platelets was significantly reduced to a similar extent through pre-incubation with both atorvastatin and simvastatin (p < 0.05). Platelets without endothelial cell contact, but in direct contact with either statin, showed similar significant reductions in surface expression of CD40L (p < 0.005).
Conclusions: These effects may explain the ability of statins to reduce the progression of atherosclerosis in addition to their cholesterol-lowering properties. (Cardiol J 2012; 19, 1: 20–28)
Abstract
Methods and Results: After a 24 h incubation period with either simvastatin or atorvastatin (1 μmol/L), human umbilical vein endothelial cells were stimulated for 1 h with lipopolysaccharide (LPS), and were then incubated in direct contact with activated platelets. Platelet surface expression of CD40L and CD62P and expression of ICAM-1, VCAM-1, uPAR and MT1-MMP on endothelial cells were measured by flow cytometry. Supernatants were analyzed by ELISA for soluble MMP-1. The increased expression of VCAM-1 and uPAR on endothelial cells by stimulation with LPS and by direct contact with activated platelets was significantly reduced to a similar extent through pre-incubation with both atorvastatin and simvastatin (p < 0.05). Platelets without endothelial cell contact, but in direct contact with either statin, showed similar significant reductions in surface expression of CD40L (p < 0.005).
Conclusions: These effects may explain the ability of statins to reduce the progression of atherosclerosis in addition to their cholesterol-lowering properties. (Cardiol J 2012; 19, 1: 20–28)
Keywords
platelets; endothelial cells; simvastatin; atorvastatin; atherosclerosis
About this articleTitle
Simvastatin and atorvastatin attenuate VCAM-1 and uPAR expression on human endothelial cells and platelet surface expression of CD40 ligand
Journal
Issue
Pages
20-28
Published online
2012-02-02
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1453
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1204
Bibliographic record
Cardiol J 2012;19(1):20-28.
Keywords
platelets
endothelial cells
simvastatin
atorvastatin
atherosclerosis
Authors
Ksenija Stach
Xuan Duc Nguyen
Siegfried Lang
Elif Elmas
Christel Weiß
Martin Borggrefe
Joachim Fischer
Thorsten Kälsch
