Jean-Michel SENARD
  • E-mail :[email]
  • Phone : 0561145961
  • Location : Toulouse, France
Last update 2011-03-30 17:17:51.586

Jean-Michel SENARD MD, PhD, Professor of pharmacology

Course and current status

ACTUALS REMITS

Status: Full Professor, Fundamental Pharmacology, University – Hospital Medical Practitioner

Teaching : Coordinator of  the pharmacology teaching and Diploma of “Délégué Médical” of the Faculty of Medicine  of Toulouse-Rangueil

Medical Care : Medical head of the Unit of Clinical Neuropharmacology and of the Laboratory of Autonomic Nervous System of the Toulouse Hospital

Research : Head of the team “Molecular and Clinical Determiants of sympathetic activity and cardiac architecture (INSERM UMR1048)

ACADEMIC REMITS

Since 1995 : Full Professor, Fundamental Pharmacology, University of Toulouse III

1991-1995: Associate Professor of Pharmacology

1987-1995 : Assistant Professor of Pharmacology

DIPLOMA

1995 : Enabling to manage a team research

1994 : Ph.D of the University of Paul Sabatier : Pharmacology Speciality : distinction with honour and jury’s congratulations.

1987 : MD. (Prix Lasserre)

1987  : DEA, Pharmacology and Molecular Toxicology, distinction with honour

1987  : Certificate of Special Studies in Neurology

Scientific summary

Despite large progresses in the treatment of cardiac diseases, morbidity and mortality still represent a huge social and economical burden making necessary to improve the efficacy of current treatments and to better understand the processes underlying the deleterious progression of these diseases. In this context, the aims of our project will be i/ to study, from molecular to clinical points of view, the pharmacological properties of molecules modulating sympathetic nervous system (SNS) activity and ii/ to delineate the role of one of the members of Eph/Ephrin family, ephrin-B1, in the heart.

i/ Hyperactivity of SNS is a well-known factor involved in the initiation, progression and outcome of cardiovascular diseases. However, drugs capable to normalize SNS activity with good efficiency are still lacking. Various explanations could account for this situation. On one hand, the molecular mechanisms whereby drugs, acting at presynaptic receptors, inhibit neurotransmitter release are not fully understood. On the other hand, their effect on SNS is only partial and often counterbalanced by a high prevalence of adverse events. The aim of this part of the project will be a/ to better understand, using BRET/FRET techniques, the molecular mechanisms whereby presynaptic receptors cooperatively modulate noradrenaline release and b/ to further investigate alterations of SNS activity in clinical settings and to assess the prognostic value of direct microneurographic measurement of muscle sympathetic nerve activity in patients with chronic heart failure.

ii/ Ephrin-B1 is a cell-cell interaction system which has been largely studied in central nervous system development, but whose role in peripheral adult tissues remains almost unknown. Our previous work on ephrin-B1 KO mice has demonstrated that this protein plays a key role in the maintenance of cardiac tissue architecture. The aim of the project will be to further characterize the role of this protein in the heart by: a/ analyzing the cardiac phenotype of efnb1-/- mice, b/ exploring its potential role in cardiomyocyte maturation, and finally, c/ studying alteration of its expression in human cardiopathies.

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