References of "Hanson, Julien"
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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 ▲]

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See detailLe bm-573, un antagoniste original de récepteur au thromboxane a2, réduit le développement des lesions atheromateuses chez des souris deficientes en apolipoproteine e (apo e-/-)
Cherdon, Céline ULg; Rolin, Stéphanie; Hanson, Julien ULg et al

Poster (2007, May 10)

Afin d’examiner l'efficacité du BM-573 dans l'athérogenèse, des souris apo E-/- ont été traitées durant 10 semaines avec le BM573 (10mg/kg). Au cours de cette expérience, le traitement des animaux par le ... [more ▼]

Afin d’examiner l'efficacité du BM-573 dans l'athérogenèse, des souris apo E-/- ont été traitées durant 10 semaines avec le BM573 (10mg/kg). Au cours de cette expérience, le traitement des animaux par le BM-573, a eu pour effet de diminuer les lésions athéromateuses précoces de manière significative. 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 synthase réduit significativement les lésions athéromateuses chez les souris apoE-/-.. Le BM-573 est, par conséquent, un agent thérapeutique potentiel pour la prévention de l'athérosclérose [less ▲]

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See detailConception et synthèse d’outils pharmacologiques originaux pour l’étude des récepteurs au thromboxane
Moray, A. L.; Dogne, J. M.; Neven, P. et al

Poster (2007, May)

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See detailCardiovascular haemodynamics and ventriculo-arterial coupling in an acute pig model of coronary ischaemia-reperfusion
Lanoye, Lieve; Segers, Patrick; Tchana-Sato, Vincent ULg et al

in Experimental Physiology (2007), 92(1), 127-137

Although reperfusion after coronary occlusion is mandatory for myocardial salvage, reperfusion may trigger a cascade of harmful events (reperfusion injury) adding to myocardial injury. We investigated ... [more ▼]

Although reperfusion after coronary occlusion is mandatory for myocardial salvage, reperfusion may trigger a cascade of harmful events (reperfusion injury) adding to myocardial injury. We investigated effects of reperfusion on left ventricular (LV) haemodynamics and ventriculo-arterial (VA) coupling in pigs following acute myocardial ischaemia induced by coronary artery occlusion. Experiments were performed in six animals, with measurements of cardiac and arterial function at baseline, after 60 min of ischaemia (T60) and after 2 (T180) and 4 h of reperfusion (T300). Ventriculo-arterial coupling was assessed using the ventriculo-arterial elastance ratio of paper, as well as using a 'stiffness coupling' and 'temporal coupling' index. Reperfusion following ischaemia (T180 versus T60) induced a progressive decline in cardiovascular function, evidenced by a decrease in mean arterial blood pressure, cardiac output and ejection fraction which was not restored at T300. Although reperfusion also induced an increase in slope of the end-systolic pressure-volume relationship (ESPVR), the ESPVR curve shifted to the right, associated with a depression of contractile function. Histology demonstrated irreversible myocardial damage at T300. The ventriculo-arterial elastance ratio and the 'stiffness coupling' index were unaffected throughout the protocol, but the 'temporal coupling' parameter indicated a relative shift between heart period and the time constant of the arterial system. It is unlikely that these alterations are attributable to ischaemic injury alone. The combination of both the stiffness and temporal coupling index may provide more information when studying ventriculo-arterial coupling than the more commonly used ventricular end-systolic stiffness/effection arterial elastance (E-es/E-a) ratio. [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

in Journal of Molecular and Cellular Cardiology (2007), 42(suppl 1.), 33-34

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See detailBM-520, an original TXA(2) modulator, inhibits the action of thromboxane A(2) and 8-iso-prostaglandin F-2 alpha in vitro and in vivo on human and rodent platelets, and aortic vascular smooth muscles from rodents
Rolin, S.; Hanson, Julien ULg; Vastersaegher, C. et al

in Prostaglandins & Other Lipid Mediators (2007), 84(1-2), 14-23

Thromboxane A(2) (TXA(2)) and 8-iso-PGF(2 alpha). are two prostanoid agonists of the thromboxane A(2) receptor (TP), whose activation has been involved in platelet aggregation and atherosclerosis. Agents ... [more ▼]

Thromboxane A(2) (TXA(2)) and 8-iso-PGF(2 alpha). are two prostanoid agonists of the thromboxane A(2) receptor (TP), whose activation has been involved in platelet aggregation and atherosclerosis. Agents able to counteract the actions of these agonists are of great interest in the treatment and prevention of cardiovascular events. Here, we investigated in vitro and in vivo the pharmacological profile of BM-520, a new TP antagonist. In our experiments, this compound showed a great binding affinity for human washed platelets TP receptors, and prevented human platelet activation and aggregation induced by U-46619, arachidonic acid and 8-iso-PGF(2 alpha). The TP receptor antagonist property of BM-520 was confirmed by its relaxing effect on rat aorta smooth muscle preparations precontracted with U-46619 and 8-iso-PGF(2 alpha). Further, its TP antagonism was also demonstrated in vivo in guinea pig after a single intravenous injection (10 mg kg(-1)). We conclude that this novel TP antagonist could be a promising therapeutic tool in pathologies such as atherosclerosis where an increased production of TXA(2) and 8-iso-PGF2., as well as TP activation are well-established pathogenic events. (c) 2007 Elsevier Inc. All rights reserved. [less ▲]

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See detailPharmacological evaluation of TP receptor antagonists by differential activity on alpha and beta isoforms
Hanson, Julien ULg; Dogne, J. M.; Ghiotto, J. et al

Poster (2006, November 18)

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See detailPharmacological evaluation of TP receptor antagonists characterized by differential activity on alpha and beta isoforms
Hanson, Julien ULg; Ghiotto, J.; Neven, P. et al

in Acta Pharmacologica Sinica (2006, July), 27

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See detailSynthesis and pharmacological evaluation of novel thromboxane modulators as antiplatelet agents acting on both the alpha and beta isoforms of the human thromboxane receptor
Hanson, Julien ULg; Reynaud, Denis; Qiao, Na et al

in Journal of Medicinal Chemistry (2006), 49(12), 3701-3709

Detailed reference viewed: 28 (15 ULg)