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HMG CoA reductase inhibitors affect the fibrinolytic system of human vascular cells in vitro: a comparative study using different statins

Wiesbauer, Franz ; Kaun, Christoph ; Zorn, Gerlinde ; Maurer, Gerald ; Huber, Kurt ; Wojta, Johann

British journal of pharmacology, 2002-01, Vol.135 (1), p.284-292 [Periódico revisado por pares]

Oxford, UK: Blackwell Publishing Ltd

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Título:
HMG CoA reductase inhibitors affect the fibrinolytic system of human vascular cells in vitro: a comparative study using different statins
Autor: Wiesbauer, Franz ; Kaun, Christoph ; Zorn, Gerlinde ; Maurer, Gerald ; Huber, Kurt ; Wojta, Johann
Assuntos: atherosclerosis ; Biological and medical sciences ; Cardiovascular system ; Cell Line ; Cell Survival - drug effects ; Cells, Cultured ; cellular ; Cholesterol - metabolism ; Coronary Vessels - drug effects ; Coronary Vessels - physiology ; cytokines ; Cytokines - metabolism ; Dose-Response Relationship, Drug ; endothelial function ; Endothelium, Vascular - cytology ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - physiology ; Experimental ; Fibrinolysis - drug effects ; Gene Expression Regulation - drug effects ; General and cellular metabolism. Vitamins ; Hepatocytes - drug effects ; Hepatocytes - physiology ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology ; Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use ; Medical sciences ; Miscellaneous ; Muscle, Smooth, Vascular - cytology ; Muscle, Smooth, Vascular - drug effects ; Muscle, Smooth, Vascular - physiology ; pathophysiology ; Pharmacology. Drug treatments ; Plasminogen Activator Inhibitor 1 - genetics ; Plasminogen Activator Inhibitor 1 - metabolism ; smooth muscle ; thrombosis ; Tissue Plasminogen Activator - genetics ; Tissue Plasminogen Activator - metabolism ; Tumor Cells, Cultured ; Umbilical Veins - drug effects ; Umbilical Veins - physiology ; vasculature
É parte de: British journal of pharmacology, 2002-01, Vol.135 (1), p.284-292
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
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Descrição: The results of several clinical studies investigating the effect of statin therapy on the fibrinolytic system in vivo are inconclusive. We compared the effect of six different statins (atorvastatin, cerivastatin, fluvastatin, lovastatin, pravastatin, simvastatin) on components of the fibrinolytic system expressed by human vascular endothelial cells and smooth muscle cells and by the human hepatoma cell line HepG2. All statins used except pravastatin significantly decreased PAI‐1 production in human endothelial and smooth muscle cells. This effect was also seen in the presence of IL‐1α and TNF‐α. All statins except pravastatin increased t‐PA production in human smooth muscle cells. On a molar basis cerivastatin was the most effective HMG CoA reductase inhibitor used. Only simvastatin and lovastatin increased t‐PA production in endothelial cells. The effects on the fibrinolytic system were reversed by mevalonate. Statins decreased mRNA levels for PAI‐1 in endothelial and smooth muscle cells and increased mRNA levels for t‐PA in smooth muscle cells. Statins did not affect PAI‐1 expression in HepG2 cells. Cell viability was not influenced by statins in endothelial cells and HepG2 cells whereas in smooth muscle cells a cytotoxic effect was seen at high concentrations. If the effects on the fibrinolytic system of vascular cells in vitro shown in this study are also operative in vivo one could speculate that by increasing t‐PA and decreasing PAI‐1 at sites of vascular lesions statins might reduce fibrin formation and thrombus development. Such an effect might contribute to the clinically proven benefits of statin therapy. British Journal of Pharmacology (2002) 135, 284–292; doi:10.1038/sj.bjp.0704454
Editor: Oxford, UK: Blackwell Publishing Ltd
Idioma: Inglês

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HMG CoA reductase inhibitors affect the fibrinolytic system of human vascular cells in vitro: a comparative study using different statins

Wiesbauer, Franz ; Kaun, Christoph ; Zorn, Gerlinde ; Maurer, Gerald ; Huber, Kurt ; Wojta, Johann

Oxford, UK: Blackwell Publishing Ltd

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