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Dive into the research topics where Liliane Tariosse is active.

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Featured researches published by Liliane Tariosse.


Cardiovascular Research | 2011

GSK-3β at the crossroads in the signalling of heart preconditioning: implication of mTOR and Wnt pathways

François Vigneron; Pierre Dos Santos; S. Lemoine; Maryline Bonnet; Liliane Tariosse; Thierry Couffinhal; Cécile Duplàa; Béatrice Jaspard-Vinassa

AIMS Ischaemic preconditioning (IPC) protects the heart against prolonged lethal ischaemia through a signalling cascade involving Akt, glycogen synthase kinase-3β (GSK-3β), and mitochondrial ATP-sensitive potassium channels (mitoK(ATP)). We previously demonstrated the involvement of the Wnt pathway in IPC in vivo via GSK-3β. A downstream target might be mammalian target of rapamycin (mTOR) since Wnt can impair tuberous sclerosis complex-2 (TSC2) phosphorylation by inhibiting GSK-3β. Here, we investigate whether the mTOR pathway is involved in cardioprotection. METHODS AND RESULTS Isolated-perfused mouse hearts were subjected to IPC via four cycles of ischaemia/reperfusion or pharmacological preconditioning (PPC) by diazoxide, a selective mitoK(ATP) activator. IPC, like PPC, induced an inhibition/phosphorylation of GSK-3β through Akt activation. Preconditioning also induced phosphorylation of mTOR, p70S6K, and 4E-BP1 that correlated with a significant reduction in infarct size after 40-min ischaemia and 120-min reperfusion when compared with non-preconditioned controls. Preconditioning was impaired in GSK3 knock-in mice. In transgenic mice hearts overexpressing secreted frizzled protein 1 (sFRP1, a Wnt/Frz antagonist), GSK-3β phosphorylation, mTOR activation, and cardioprotection were impaired. Cardioprotection and its signalling were also inhibited by rapamycin (an mTOR inhibitor), 5-HD (a mitoK(ATP) blocker), and N-(2-mercaptopropionyl) glycine (MPG) as a reactive oxygen species (ROS) scavenger. CONCLUSIONS We propose that the preconditioning signalling pathway involving an amplification loop results in a downregulation of GSK-3β and a constant opening of mitoK(ATP) with ROS generation to activate the mTOR pathway and induce cardioprotection. The disruption of the Wnt/Frz pathway by sFRP1 modulates this loop, inducing GSK-3β activation. This study provides evidence that cardioprotection involves both a pro-survival mTOR pathway and a developmental Wnt pathway targeting GSK-3β.


British Journal of Pharmacology | 1996

Development of the model of rat isolated perfused heart for the evaluation of anthracycline cardiotoxicity and its circumvention

Paul Pouna; Simone Bonoron-Adèle; Gérard Gouverneur; Liliane Tariosse; P. Besse; Jacques Robert

1 In order to develop a predictive model for the preclinical evaluation of anthracycline cardiotoxicity and the means of preventing it, we have studied the functional parameters of perfused hearts isolated from rats receiving repeated doses of several anthracyclines. 2 The anthracyclines studied were doxorubicin, epirubicin, pirarubicin and daunorubicin, and we also studied a liposomal formulation of daunorubicin (DaunoXome) and the co‐administration of dexrazoxane (ICRF‐187) and doxorubicin. 3 Anthracyclines were administered i.p. at equimolar doses corresponding to 3 mg kg−1 per injection of doxorubicin, every other day for a total of six doses. Dexrazoxane was used at the dose of 30 mg kg−1 per injection and was administered either 30 min before or 30 min after doxorubicin. We evaluated any general toxicity towards the animals as well as alterations of left ventricular contractility and relaxation ex vivo. 4 Epirubicin and daunorubicin were significantly less cardiotoxic than doxorubicin, and neither pirarubicin nor DaunoXome caused significant alterations in cardiac function. There was a direct relationship between the decrease in cardiac contractility or relaxation and anthracycline accumulation in the heart, evaluated after the same treatment schedule. 5 Dexrazoxane induced a significant protection against doxorubicin‐induced cardiac toxicity when administered 30 min before doxorubicin, whereas this protection was ineffective when administered 30 min after doxorubicin. Direct perfusion of DaunoXome in isolated hearts of untreated animals resulted in a 12‐fold reduction of the accumulation of daunorubicin in heart tissue as compared to the perfusion of free daunorubicin, and did not cause alterations in cardiac function at a dosage for which free daunorubicin induced major alterations. 6 The isolated perfused rat heart appears to be a valuable model for screening of new anthracyclines and of strategies for circumventing anthracycline cardiotoxicity.


American Journal of Physiology-heart and Circulatory Physiology | 2008

Effect of diazoxide on flavoprotein oxidation and reactive oxygen species generation during ischemia-reperfusion: a study on Langendorff-perfused rat hearts using optic fibers

Philippe Pasdois; Bertrand Beauvoit; Liliane Tariosse; Béatrice Vinassa; Simone Bonoron-Adèle; Pierre Dos Santos

This study analyzed the oxidant generation during ischemia-reperfusion protocols of Langendorff-perfused rat hearts, preconditioned with a mitochondrial ATP-sensitive potassium channel (mitoK(ATP)) opener (i.e., diazoxide). The autofluorescence of mitochondrial flavoproteins, and that of the total NAD(P)H pool on the one hand and the fluorescence of dyes sensitive to H(2)O(2) or O(2)(*-) [i.e., the dihydrodichlorofluoroscein (H(2)DCF) and dihydroethidine (DHE), respectively] on the other, were noninvasively measured at the surface of the left ventricular wall by means of optic fibers. Isolated perfused rat hearts were subjected to an ischemia-reperfusion protocol. Opening mitoK(ATP) with diazoxide (100 microM) 1) improved the recovery of the rate-pressure product after reperfusion (72 +/- 2 vs. 16.8 +/- 2.5% of baseline value in control group, P < 0.01), and 2) attenuated the oxidant generation during both ischemic (-46 +/- 5% H(2)DCF oxidation and -40 +/- 3% DHE oxidation vs. control group, P < 0.01) and reperfusion (-26 +/- 2% H(2)DCF oxidation and -23 +/- 2% DHE oxidation vs. control group, P < 0.01) periods. All of these effects were abolished by coperfusion of 5-hydroxydecanoic acid (500 microM), a mitoK(ATP) blocker. During the preconditioning phase, diazoxide induced a transient, reversible, and 5-hydroxydecanoic acid-sensitive flavoprotein and H(2)DCF (but not DHE) oxidation. In conclusion, the diazoxide-mediated cardioprotection is supported by a moderate H(2)O(2) production during the preconditioning phase and a strong decrease in oxidant generation during the subsequent ischemic and reperfusion phases.


Cancer Chemotherapy and Pharmacology | 1995

Evaluation of anthracycline cardiotoxicity with the model of isolated, perfused rat heart: comparison of new analogues versus doxorubicin

Paul Pouna; Simone Bonoron-Adèle; Gérard Gouverneur; Liliane Tariosse; P. Besse; Jacques Robert

We have compared the cardiotixicity of 3 anthracyclines in a model of isolated perfused rat heart using the Langendorff technique. The contractile state and ventricular compliance were studied. Doxorubicin, epirubicin and pirarubicin were perfused at concentrations of 10−6 and 10−5 M during 70 min. The cardiac accumulation of the drugs was studied by HPLC. No significant alteration of cardiac functional parameters was observed at 10−6 M. At 10−5 M, epirubicin produced a significantly greater alteration of cardiac contractility than doxorubicin, whereas pirarubicin exerted first an inotropic effect followed by a recovery to initial values at the 60th min. Anthracycline accumulation in the heart was dose-dependent; epirubicin accumulated to a 30% greater extent than doxorubicin and pirarubicin heart concentrations were 4–5 times higher than those of doxorubicin at the end of the perfusion. These results suggest that doxorubicin and epirubicin have the same intrinsic cardiac toxicity, and that their distinct clinical cardiotoxicity must be explained by pharmacokinetic differences, whereas pirarubicin is much less cardiotoxic than the other anthracyclines because of different pharmacodynamic properties.


Journal of Cardiovascular Electrophysiology | 2006

Effects of Right, Left, and Biventricular Pacing on Myocardial Perfusion in Ischemic Conditions

S. Lafitte; Patricia Reant; Louis Labrousse; Pierre Bordachar; Liliane Tariosse; Bertrand Beauvoit; Karim Serri; Simone Bonoron-Adèle; Raymond Roudaut; Pierre Dos Santos

Objectives: In normal hearts, the distribution of regional myocardial perfusion is altered by ventricular pacing. Little is known about the impact of ventricular pacing on regional myocardial perfusion in ischemic conditions. In this acute echocardiographic study, we compared the respective effects of right ventricular pacing (RVP), left ventricular pacing (LVP), and biventricular pacing (BVP) on regional perfusion in a swine model of graded ischemia.


American Journal of Physiology-heart and Circulatory Physiology | 2002

Mechanisms by which opening the mitochondrial ATP- sensitive K+ channel protects the ischemic heart

Pierre Dos Santos; Alicia J. Kowaltowski; Muriel N. Laclau; Subramanian Seetharaman; Petr Paucek; Sihem Boudina; Jean Benoit Thambo; Liliane Tariosse; Keith D. Garlid


American Journal of Physiology-heart and Circulatory Physiology | 2007

Ouabain protects rat hearts against ischemia-reperfusion injury via pathway involving src kinase, mitoKATP, and ROS

Philippe Pasdois; Casey L. Quinlan; Abraham Rissa; Liliane Tariosse; Béatrice Vinassa; Alexandre D. T. Costa; Sandrine V. Pierre; Pierre Dos Santos; Keith D. Garlid


American Journal of Physiology-heart and Circulatory Physiology | 2002

Alteration of mitochondrial function in a model of chronic ischemia in vivo in rat heart

Sihem Boudina; Muriel N. Laclau; Liliane Tariosse; Danièle Daret; Gérard Gouverneur; Simone Bonoron-Adèle; Valdur Saks; Pierre Dos Santos


American Journal of Physiology-heart and Circulatory Physiology | 2006

Inhibition of cardiac contractility by 5-hydroxydecanoate and tetraphenylphosphonium ion: a possible role of mitoKATP in response to inotropic stress.

Keith D. Garlid; Paolo Emilio Puddu; Philippe Pasdois; Alexandre D. T. Costa; Bertrand Beauvoit; Anna Criniti; Liliane Tariosse; Philippe Diolez; Pierre Dos Santos


Journal of Molecular and Cellular Cardiology | 2007

Sarcoplasmic ATP-sensitive potassium channel blocker HMR1098 protects the ischemic heart: Implication of calcium, complex I, reactive oxygen species and mitochondrial ATP-sensitive potassium channel

Philippe Pasdois; Bertrand Beauvoit; Alexandre D. T. Costa; Béatrice Vinassa; Liliane Tariosse; Simone Bonoron-Adèle; Keith D. Garlid; Pierre Dos Santos

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Keith D. Garlid

Portland State University

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Abraham Rissa

Portland State University

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