References of "Ooms, Annie"
     in
Bookmark and Share    
Full Text
Peer Reviewed
See detailSynthesis and pharmacological evaluation of 2-aryloxy/arylamino-5-cyanobenzenesulfonylureas as novel thromboxane A2 receptor antagonists
Bambi-Nyanguile, Sylvie-Mireille; Hanson, Julien ULg; OOMS, Annie ULg et al

in European Journal of Medicinal Chemistry (2013), 65C

Detailed reference viewed: 32 (7 ULg)
Full Text
Peer Reviewed
See detailBM-573 INHIBITS THE EARLY ATHEROSCLEROTIC LESIONS IN APO-E DEFICIENT MICE BY BLOCKING TP RECEPTORS AND THROMBOXANE SYNTHASE
Cherdon, Céline ULg; Rolin, Stéphanie; Hanson, Julien ULg et al

in Congress of the International Society of Thrombosis and Hemostasis- 57th Annual SSC Meeting (2011, July)

Atherosclerosis is the principal cause of mortality in industrialized countries. Its development is influenced by several mediators of which thromboxane A(2) (TXA(2)) and 8-iso-PGF(2() have recently ... [more ▼]

Atherosclerosis is the principal cause of mortality in industrialized countries. Its development is influenced by several mediators of which thromboxane A(2) (TXA(2)) and 8-iso-PGF(2() have recently received a lot of attention. This study aimed to investigate the effect of a dual thromboxane synthase inhibitor and thromboxane receptor antagonist (BM-573) and ASA on lesion formation in apolipoprotein E-deficient mice. The combination of ASA and BM-573 was also studied. Plasma measurements demonstrated that the treatments did not affect body weight or plasma cholesterol levels. BM-573, but not ASA, significantly decreased atherogenic lesions as demonstrated by macroscopic analysis. Both treatments alone inhibited TXB(2) synthesis but only BM-573 and the combination therapy were able to decrease firstly, plasma levels of soluble intracellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) and secondly, the expression of these proteins in the aortic root of Apo E. These results were confirmed in endothelial cell cultures derived from human saphenous vein endothelial cells (HSVECs). In these cells, BM-573 also prevented the increased mRNA expression of ICAM-1 and VCAM-1 induced by U-46619 and 8-iso-PGF(2(). Our results show that a molecule combining receptor antagonism and thromboxane synthase inhibition is more efficient in delaying atherosclerosis in Apo E(-/-) mice than sole inhibition of TXA(2) formation. [less ▲]

Detailed reference viewed: 61 (10 ULg)
Full Text
Peer Reviewed
See detailBM-573 inhibits the development of early atherosclerotic lesions in Apo E deficient mice by blocking TP receptors and thromboxane synthase.
Cherdon, Céline ULg; Rolin, Stephanie; Hanson, Julien ULg et al

in Prostaglandins & Other Lipid Mediators (2011)

Atherosclerosis is the principal cause of mortality in industrialized countries. Its development is influenced by several mediators of which thromboxane A(2) (TXA(2)) and 8-iso-PGF(2() have recently ... [more ▼]

Atherosclerosis is the principal cause of mortality in industrialized countries. Its development is influenced by several mediators of which thromboxane A(2) (TXA(2)) and 8-iso-PGF(2() have recently received a lot of attention. This study aimed to investigate the effect of a dual thromboxane synthase inhibitor and thromboxane receptor antagonist (BM-573) and ASA on lesion formation in apolipoprotein E-deficient mice. The combination of ASA and BM-573 was also studied. Plasma measurements demonstrated that the treatments did not affect body weight or plasma cholesterol levels. BM-573, but not ASA, significantly decreased atherogenic lesions as demonstrated by macroscopic analysis. Both treatments alone inhibited TXB(2) synthesis but only BM-573 and the combination therapy were able to decrease firstly, plasma levels of soluble intracellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) and secondly, the expression of these proteins in the aortic root of Apo E. These results were confirmed in endothelial cell cultures derived from human saphenous vein endothelial cells (HSVECs). In these cells, BM-573 also prevented the increased mRNA expression of ICAM-1 and VCAM-1 induced by U-46619 and 8-iso-PGF(2(). Our results show that a molecule combining receptor antagonism and thromboxane synthase inhibition is more efficient in delaying atherosclerosis in Apo E(-/-) mice than sole inhibition of TXA(2) formation. [less ▲]

Detailed reference viewed: 54 (8 ULg)
Full Text
Peer Reviewed
See detailThe use of an adapted model allows contributing to the “Reduction” of mice used in experimental protocols: the case of the apoE–deficient (apo E-/-) mice in a model of atherosclerosis control
Cherdon, Céline ULg; Rolin, Stéphanie; de Leval, Laurence ULg et al

Poster (2009, December 01)

Atherosclerosis is a chronic vascular disease whose development is influenced by several mediators 1. Among them, the prostanoids large family lipids generated from the metabolism of arachidonic acid by ... [more ▼]

Atherosclerosis is a chronic vascular disease whose development is influenced by several mediators 1. Among them, the prostanoids large family lipids generated from the metabolism of arachidonic acid by the action of COX includes various types of PGs and thromboxane. Thromboxane A2 and PGI2 are present in abnormally elevated concentration in atherosclerosis 2-3. To exert its effects TXA2 and its precursor PGH2 act at a specific receptor termed TP receptor 4. As a result, TXA2 synthase inhibitors and TP antagonists have been developed to reduce and to prevent TXA2 production and actions, respectively. The present study was undertaken in order to investigate whether BM-573, an original sulfonylurea derivate synthesized in our lab 5, and aspirin would be effective in preventing the progression of atherosclerosis in an apo E deficient mouse model. [less ▲]

Detailed reference viewed: 56 (14 ULg)
Full Text
Peer Reviewed
See detailLe bm-573, un antagoniste original du récepteur au thromboxane a2, réduit le développement des lésions athéromateuses chez des souris déficientes en apolipoprotéine e (apo e-/-) contrairement a l’aspirine.
Cherdon, Céline ULg; Rolin, Stéphanie; Ooms, Annie ULg et al

(2009, May 28)

Afin d’examiner l'efficacité de l’aspirine et du BM-573 dans l'athérogenèse, des souris apo E-/- femelles ont été traitées durant 10 et 20 semaines avec le BM-573 (10mg/kg/j), l’aspirine (30mg/kg/j) ou un ... [more ▼]

Afin d’examiner l'efficacité de l’aspirine et du BM-573 dans l'athérogenèse, des souris apo E-/- femelles ont été traitées durant 10 et 20 semaines avec le BM-573 (10mg/kg/j), l’aspirine (30mg/kg/j) ou un placébo. Au cours de cette expérience, aucune modification du poids corporel ou de la cholestérolémie n’a été observée. Par contre, le traitement des animaux par le BM-573, a eu pour effet de diminuer les lésions athéromateuses de manière significative tandis que l’aspirine a été sans effet sur ce paramètre. Ces données ont été confirmées par des analyses histopathologiques et biochimiques. Ces résultats confirment que l'antagonisme sélectif des récepteurs TP associé à une inhibition de la thromboxane synthétase réduit significativement les lésions athéromateuses chez les souris apo E-/-. Le BM-573 est, par conséquent, un agent thérapeutique potentiel pour la prévention de l'athérosclérose. [less ▲]

Detailed reference viewed: 42 (12 ULg)