Catherine Coirault
  • E-mail :[email]
  • Phone : +33 1 42 16 57 55
  • Location : Paris, France
Last update 2011-05-25 06:36:55.022

Catherine Coirault MD-PhD Pathophysiology of Striated muscle

Course and current status

Academic Position

Researcher: CR1 INSERM since October 1998

Laboratory of “Therapy of striated muscle diseases” directed by Thomas Voit, UMRS_974 Inserm UPMC, UMR 7215 CNRS, Institut de Myologie, 47 bld de l’Hôpital, GH Pitié-Salpétrière, Paris, France.

Member of Team 1 “Genetics & Pathophysiology of Neuromuscular Disorders”.


1993: Doctor in Medicine (MD degree). Faculty of Medicine, Paris 11.

1993: Specialization obtained in Cardio-Vascular Pathologies (Cochin-Port Royal Faculty, Paris).

1995: Doctor of Science (PhD) "Mechanics and energetics of the diaphragmatic muscle". Paris 11

1997: HDR (Habilitation to lead research programs), Physiology, Paris 11.

Scientific Research Experiences

1991-1992: Sabbatical year of research

1992-1995: Doctorat en Sciences: Mechanics and energetics of diaphragm muscle.

1996-1998: Post doctoral fellow: INSERM, Ecole Polytechnique, Palaiseau). “Regulation of actin-myosin interactions in striated and smooth muscles”

1998: Research Associate CR1 INSERM

1999: Post-doctorant fellow in York (GB): Justin Molloy’s Muscle Lab.

2000-2003: Head of the Inserm biomedical team “Actin-myosin interactions and contractile dysfunction”, Inserm U451, Palaiseau. Lab. director: Prof JL Martin.

2003–2006: Head of the Inserm team “Actomyosin interactions in chronic heart failure”, Inserm U572, Lariboisière Hospital, Paris. Lab Director: Dr JL Samuel.

2003-2006: Principal coordinator of a French multidisciplinary project on ARVD (rare disease project granted by GIS-INSERM-AFM) including 10 hospital departments (clinical, genetics and researchers).

2006-July 2007: Head of Inserm team “Cellular & molecular Physiopathology in heart failure” in U689, CRCIL- U689 (Hôpital Lariboisière, Paris). Laboratory director: Prof. B. Levy.

2007-present: Leader of the group “Physiopathology of contractile dysfunction” in Team 1 directed by G Bonne.


Recipient of the award of the Assistance Publique-Hôpitaux de Paris (Médaille d'or) – 1993.

Scientific summary

The project of our group focuses on the pathophysiology of the contractile dysfunction of striated muscles. Many neuromuscular disorders are associated with contractile dysfunction, reduced adaptability of the muscular cells to respond to a mechanical stress and/or activation of intracellular signalling pathways which modulate their phenotypical expression. Mechanisms by which cells convert mechanical signals into biochemical responses involve complex interactions between cell-ECM (integrins, focal adhesions) and cell-cell adhesions (cadherins), the extracellular matrix (fibronectin, collagen, proteoglycans…), cytoskeleton (intermediate filaments, microtubules…), nuclear structures (lamins, chromatin, gene expression…) and the contractile machinery. They are called mechano-transduction. It remains challenging for the future to identify biomechanical factors and to determine their contributions in neuromuscular disorders.

Our purpose is to better understand the pathophysiology of the contractile dysfunction and more precisely, the role of cell-extracellular matrix interactions in the onset and maintenance of the contractile dysfunction in different muscular disorders.

In addition to the analysis of the mechanical function of isolated muscles from various animal models, we have developed 3D cultures of myoblasts so as to obtain artificial contractile tissues (3D culture with normal & pathological human/murine myoblasts). Such 3D tools seem particularly relevant in the muscle field because they make it possible i) to precisely control the forces exerted on and by the muscular cells on the ECM (activation/inhibition of contraction, tissue strain culture system, ii) to modulate cell-ECM adhesion (binding of peptides that modulate the organisation/activity of integrins (RGD, RGE) or other receptors…), iii) to modulate the ECM composition (COL6 deficient cells for example), the intracellular cytoskeleton (cells expressing lamins A/C or desmin mutations…) and/or the intracellular signalling pathways (modulation of the ERK MAPK and Akt pathways by adenovirus or siRNA transfections). Our aim is to analyze contractile function (force & length microtransducer), cytoskeleton/contractile proteins/nucleus interactions (IF, IP) and the markers of intracellular signalling pathway (qRT-PCR, WB, IF) in normal and pathological contexts of proliferation/ differentiation. In addition, we performed in vitro motility assays to investigate contractile function at the molecular level (actin-myosin interactions).

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