Jacques Noireaud
  • E-mail :[email]
  • Phone : 33 6 15 20 04 20
  • Location : Angers, France
Last update 2012-01-21 10:29:49.153

Jacques Noireaud In vitro functional studies in adult cardiomyocytes

Course and current status

Dr. Jacques Noireaud holds a Doctorat of Speciality Animal Physiology, from the University of Poitiers (France), since 1977 and a Doctorat of State es’Sciences, from the University of Nantes (France), since 1985. His post-doctoral experiences in the Department of Physics of the University of Calgary (Canada, 1978-79), the Department of Physiology I of the University of Homburg (Allemagne, 1980-81) and the Department of Physiology of the University Medical School of Edinburgh (GB, 1984-86), and his collaborations with the laboratory of Aarhus (Danemark, 1996-97), the department of Molecular Cardiology of Freiburg (Allemagne, 1998) and the laboratory of Gene Therapy of Nantes (2000), led him to built his expertise in the regulation of contractility, electrophysiology, receptology and intracellular ion homeostasis in cardiac, skeletal and vascular muscles, mainly using in vitro approaches.

On 1986, he joined the INSERM as “Chargé de Recherche” and became Director of Research on 1992. In Nantes (France), he successively carried out his research activities in the laboratory of General Physiology (URA CNRS 1340, 1986-1992) and the laboratory of Experimental Cardiology (1993-1995) which is at the origin of a “Contrat Jeune Formation” INSERM labellisation (1996-99), the INSERM Unit 533 (2000-2003), then Unit 915 (“Institut du Thorax”, 2004-2007). During the period 2008-2010, he worked in the laboratory of Animal Physiopathology and Functional Pharmacology (UPSP 5304) of Oniris (previously called the National Veterinary School) in Nantes (France).

Finally, on 2011, he joined the Inserm UMR 694 (on 2012 : Inserm UMR 1063) in Angers in order to bring over his skill upon fonctional studies (cell shortening and calcium transient) in isolated cardiomyocytes of adult mammalian heart in a laboratory whose researches mainly focuse on translational research depicting the role of oxidative stress in metabolic diseases (metabolic syndrome, obesity, obstructive sleep apnea-hypopnea syndrome, diabetes) with special interest in circulating microparticles, mitochondrial function and polyphenols.

On 1997, he became a member of The Physiological Society and of the “Société Française de Cardiology” and on 2007 of the “Société Française de Pharmacologie et de Thérapeuthique”. He has authored over 56 scientific articles in peer-reviewed publications.

Scientific summary

Recent interesting data : (1) In a study published on 2009, we provided the first comprehensive characterization of the functional expression of β3-adrenoceptors (AR) in rabbit cardiomyocytes. We showed that β3-AR stimulation induced (1) a negative inotropic effect associated to a reduction in Ca2+ transient and ICa,L current amplitudes and (2) a positive lusitropic effect in agreement with an increase in IKs current amplitude and finally (3) an acceleration of the action potential repolarisation. All these functional effects induced by β3-AR stimulation were specific of β3-AR and involved activation of Gi and NO pathways. Thus, rabbit heart represents a good model to explore the possibility that β3-AR could represent a new anti-arrhythmic target by (i) decreasing Ca2+ overload by preventing increased Ca2+ influx via the L-type Ca2+ channel and (ii) preventing prolongation of ventricular repolarisation in heart failure by activation of K+ channels.

(2) Circulating autoantibodies directed against β1-AR (β1-AAB) have been detected in the serum of patients with various cardiovascular pathologies. In mammalian heart, the β1-AR can exist in two distinct activated conformations (so-called high- and low-affinity states). We have recently showed and communicated that in rat cardiomyocytes, β1-AAB have no agonist/antagonist-like effects upon the low-affinity state of the β1-AR. Concerning cardiac pathogenesis, such as dilated cardiomyopathy, where sustained β1-AR activation is present and achieved by stimulatory β1-AAB, our work suggests that the low-affinity state of β1-AR might not be implicated in the potential harmful effects of that overactivation.

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