References of "Hanson, Julien"
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See detailHeterologously expressed formyl peptide receptor 2 (FPR2/ALX) does not respond to lipoxin A4
Hanson, Julien ULg; Ferreiros, Nerea; Pirotte, Bernard ULg et al

in Biochemical Pharmacology (2013), 85

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See detailDevelopment of original 2-aryloxy/arylamino-5-cyanobenzenesulfonylureas as thromboxane A2 receptor antagonists
Bambi Nyanguile, Sylvie-Mireille ULg; Hanson, Julien ULg; Dogné, Jean-Michel et al

Poster (2012, August)

A series of novel 2-aryloxy/arylamino-5-cyanobenzenesulfonylureas were synthesized. The newly synthesized compounds were tested in vitro and ex vivo as thromboxane A2 receptor antagonists. Some of the ... [more ▼]

A series of novel 2-aryloxy/arylamino-5-cyanobenzenesulfonylureas were synthesized. The newly synthesized compounds were tested in vitro and ex vivo as thromboxane A2 receptor antagonists. Some of the test compounds showed potent thromboxane A2 receptor antagonist activity. Three compounds (7h, 8h and 8e) were identified as leads for further pharmacological and toxicological studies. [less ▲]

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See detailRole of HCA₂ (GPR109A) in nicotinic acid and fumaric acid ester-induced effects on the skin
Hanson, Julien ULg; Gille, Andreas; Offermanns, Stefan

in Pharmacology & Therapeutics (2012)

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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 ▲]

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See detailMechanism of Nicotinic acid-induced Flushing
Hanson, Julien ULg

Conference (2011, June 10)

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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 ▲]

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See detailNicotinic acid (niacin): new lipid-independent mechanisms of action and therapeutic potentials
lukasova, Martina; Hanson, Julien ULg; Tunaru, Sorin et al

in Trends in Pharmacological Sciences (2011)

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See detailRole of Keratinocytes GPR109A and COX-2 in Nicotinic Acid and Mono-methyl Fumarate Induced Flushing
Hanson, Julien ULg; Gille, Andreas; Zwykiel, Sabrina et al

Poster (2010, July 17)

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See detailNicotinic acid- and monomethyl fumarate-induced flushing involves GPR109A expressed by keratinocytes and COX-2-dependent prostanoid formation in mice.
Hanson, Julien ULg; Gille, Andreas; Zwykiel, Sabrina et al

in Journal of Clinical Investigation (2010), 120(8), 2910-9

The antidyslipidemic drug nicotinic acid and the antipsoriatic drug monomethyl fumarate induce cutaneous flushing through activation of G protein-coupled receptor 109A (GPR109A). Flushing is a troublesome ... [more ▼]

The antidyslipidemic drug nicotinic acid and the antipsoriatic drug monomethyl fumarate induce cutaneous flushing through activation of G protein-coupled receptor 109A (GPR109A). Flushing is a troublesome side effect of nicotinic acid, but may be a direct reflection of the wanted effects of monomethyl fumarate. Here we analyzed the mechanisms underlying GPR109A-mediated flushing and show that both Langerhans cells and keratinocytes express GPR109A in mice. Using cell ablation approaches and transgenic cell type-specific GPR109A expression in Gpr109a-/- mice, we have provided evidence that the early phase of flushing depends on GPR109A expressed on Langerhans cells, whereas the late phase is mediated by GPR109A expressed on keratinocytes. Interestingly, the first phase of flushing was blocked by a selective cyclooxygenase-1 (COX-1) inhibitor, and the late phase was sensitive to a selective COX-2 inhibitor. Both monomethyl fumarate and nicotinic acid induced PGE2 formation in isolated keratinocytes through activation of GPR109A and COX-2. Thus, the early and late phases of the GPR109A-mediated cutaneous flushing reaction involve different epidermal cell types and prostanoid-forming enzymes. These data will help to guide new efficient approaches to mitigate nicotinic acid-induced flushing and may help to exploit the potential antipsoriatic effects of GPR109A agonists in the skin. [less ▲]

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See detailAn autocrine lactate loop mediates insulin-dependent inhibition of lipolysis through GPR81.
Ahmed, Kashan; Tunaru, Sorin; Tang, Cong et al

in Cell Metabolism (2010), 11(4), 311-9

Lactate is an important metabolic intermediate released by skeletal muscle and other organs including the adipose tissue, which converts glucose into lactate under the influence of insulin. Here we show ... [more ▼]

Lactate is an important metabolic intermediate released by skeletal muscle and other organs including the adipose tissue, which converts glucose into lactate under the influence of insulin. Here we show that lactate activates the G protein-coupled receptor GPR81, which is expressed in adipocytes and mediates antilipolytic effects through G(i)-dependent inhibition of adenylyl cyclase. Using GPR81-deficient mice, we demonstrate that the receptor is not involved in the regulation of lipolysis during intensive exercise. However, insulin-induced inhibition of lipolysis and insulin-induced decrease in adipocyte cAMP levels were strongly reduced in mice lacking GPR81, although insulin-dependent release of lactate by adipocytes was comparable between wild-type and GPR81-deficient mice. Thus, lactate and its receptor GPR81 unexpectedly function in an autocrine and paracrine loop to mediate insulin-induced antilipolytic effects. These data show that lactate can directly modulate metabolic processes in a hormone-like manner, and they reveal a new mechanism underlying the antilipolytic effects of insulin. [less ▲]

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See detailDeorphanization of GPR109B as a receptor for the beta-oxidation intermediate 3-OH-octanoic acid and its role in the regulation of lipolysis
Ahmed, Kashan; Tunaru, Sorin; Langhans, C. D. et al

in Journal of Biological Chemistry (2009), 284(33), 21928-33

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See detailBm-573, an original thromboxane receptor antagonist, reduces development of atherosclerosis in apoe–deficient (apo e-/-) mice
Cherdon, Céline ULg; Rolin, Stéphanie; Hanson, Julien ULg et al

Poster (2007, October 11)

To test the efficacy of BM-573 in atherogenesis, the effect of 10 weeks of treatment with BM573 (10 mg/l) on early aortic atherosclerotic lesions of apo E deficient mice was assessed. These mice were fed ... [more ▼]

To test the efficacy of BM-573 in atherogenesis, the effect of 10 weeks of treatment with BM573 (10 mg/l) on early aortic atherosclerotic lesions of apo E deficient mice was assessed. These mice were fed with chow diet, with spontaneous increase of total plasma cholesterol and triglycerides. In this experiment, while BM-573 did not affect body weight, it significantly decreases early atherogenesis lesions confirmed by macroscopic, microscopic and biochemical analysis. These results confirm that selective antagonism of TP receptor is effective in reducing atherosclerotic lesion in apo E deficient mice. Consequently, BM-573 could be a potential drug for prevention of atherosclerosis [less ▲]

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See detailBm-573, a thromboxane receptor antagonist, reduces development of atherosclerosis in apoe–deficient mice
Cherdon, Céline ULg; Rolin, Stéphanie; Hanson, Julien ULg et al

Poster (2007, June 22)

Atherosclerotic cardiovascular disease, according to World Health Organization, is the primary cause of heart disease and stroke. Atherosclerosis is a chronic vascular disease whose development is ... [more ▼]

Atherosclerotic cardiovascular disease, according to World Health Organization, is the primary cause of heart disease and stroke. Atherosclerosis is a chronic vascular disease whose development is influenced by several mediators. Among them, the action of eicosanoïds such as thromboxane A2 and 8-iso-PGF2a have recently received a lot of attention. The aim of our study was the evaluation of benefits of original molecules, synthesised in our lab, targeting the thromboxane receptor (TP) in an apo E deficient mouse. We previously demonstrated in several in vitro and in vivo pharmacological experiments that our original sulfonylurea derivate, BM-573 was a potent combined inhibitor of the thromboxane synthase and antagonist of TP. Since TP is implied in atherosclerosis development, such antagonist could have a great therapeutic impact in atherogenesis.To test the efficacy of BM-573 in atherogenesis, the effect of 10 weeks of treatment with BM573 (10 mg/kg) on early aortic atherosclerotic lesions of apo E deficient mice was assessed. These mice were fed with chow diet, with spontaneous increase of total plasma cholesterol and triglycerides. In this experiment, while BM-573 did not affect body weight, it significantly decreased early atherogenesis lesions confirmed by macroscopic, microscopic and biochemical analysis. These results confirm that selective antagonism of TP receptor is effective in reducing atherosclerotic lesion in apo E deficient mice. Consequently, BM-573 could be a potential drug for prevention of atherosclerosis. [less ▲]

Detailed reference viewed: 55 (9 ULg)