- Habilitation à Diriger les Recherches (HDR); Paris XI; 1999
- PhD; Paris XI (Orsay); 1988
- Master degree in "Fundamental and Applied Toxicology"; Paris VII; 1985
- Master degree in "Animal Biology and Physiology"; Paris XI (Orsay); 1984
Head of the INSERM Unit "Cellular interactions and liver physiopathology". Created the 1st January 2015
Head of the INSERM Unit "Calcium Signaling and cellular interactions in the liver" (2006-2014)
-Research director: (DR2) INSERM since April 2000
-Researcher: (CR1) INSERM April 1993 - 2000
(CR2) INSERM April 1989 - 1993
-Visiting scientist; University of Cambridge; September 1993 - November 1994
-F.R.M. funding November 1988 - April 1989
-M.R.T funding October 1985 - September 1988
We investigate the cell biology and pathophysiology of liver diseases and related biological processes using an interdisciplinary approach ranging from biophysics and biochemistry to biology and the clinics. The members of the laboratory have complementary expertise in these diverse fields.
An important, although largely unexplored feature is that after injury and during liver repair, liver functions have to be maintained to fulfill the peripheral demand. This is particularly critical for bile secretion, which has to be finely tuned in order to preserve liver parenchyma from bile-induced injury. However, mechanisms allowing the liver to maintain biliary homeostasis during repair after injury are not completely understood. Part of the lab studies the impact of purinergic and bile acid signalling in liver repair and biliary homeostasis.
During chronic cholestatic liver diseases, prolonged exposure of the parenchyma to high bile acid levels, such as occurring in particular during progressive familial intrahepatic cholestasis (mainly PFIC2), is associated with bile acid-induced tissue damage, portal inflammation, and high risk of hepatobiliary malignancy. Another part of our lab studies the PFIC2 pathophysiology and treatment.
It is also important to keep in mind that, in conditions of chronic liver injury or if submassive liver cell loss occurs, regenerative capacity for hepatocyte self-renewal can be overwhelmed, potentially leading to liver failure. In those conditions, liver progenitor cells (LPC), which are dormant and found in the periportal area in the normal liver, actively proliferate and constitute the so-called “ductular reaction”. It is thought that LPC contribute to the maintenance of liver mass homeostasis in those extreme conditions, giving rise to both hepatocytes and cholangiocytes, through yet incompletely determined mechanisms. The maintenance of biliary homeostasis during liver regeneration and repair thus also depends on this process and in particular on cholangiocyte differenciation. Our lab is working on ciliary proteins and cholangiocyte differentiation.