Regulation of thrombomodulin expression in human vascular smooth muscle cells by COX-2-derived prostaglandins.
Circ Res
; 96(1): e1-6, 2005 Jan 07.
Article
en En
| MEDLINE
| ID: mdl-15591227
ABSTRACT
There is concern that cyclooxygenase (COX)-2 inhibitors may promote atherothrombosis by inhibiting vascular formation of prostacyclin (PGI2) and an increased thrombotic risk of COX-2 inhibitors has been reported. It is widely accepted that the prothrombotic effects of COX-2 inhibitors can be explained by the removal of platelet-inhibitory PGI2. Using microarray chip technology, we have previously demonstrated that thrombomodulin (TM) mRNA is upregulated in cultured human coronary artery smooth muscle cells by the stable prostacyclin mimetic iloprost. This study is the first to demonstrate a stimulation of the expression of functionally active thrombomodulin in human smooth muscle cells by prostaglandins, endogenously formed via the COX-2 pathway. Because TM is an important inhibitor of blood coagulation, these findings provide a novel platelet-independent mechanism to explain the prothrombotic effects of COX-2 inhibitors. The full text of this article is available online at http//circres.ahajournals.org.
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Bases de datos:
MEDLINE
Asunto principal:
Piridinas
/
Sulfonas
/
Alprostadil
/
Regulación de la Expresión Génica
/
Epoprostenol
/
Inhibidores de la Ciclooxigenasa
/
Prostaglandina-Endoperóxido Sintasas
/
Trombomodulina
/
Trombofilia
/
Miocitos del Músculo Liso
Tipo de estudio:
Prognostic_studies
Idioma:
En
Revista:
Circ Res
Año:
2005
Tipo del documento:
Article
País de afiliación:
Alemania