PhD: 1982. Prepared in CNRS LA 244, Claude Bernard University / Lyon I. Field: Morphophysiology of invertebrate smooth muscle cells.
1983 to 1986 : Research scientist in the "Centre de recherche en Rhumatologie", Edouard Herriot hospital, Lyon, France. Validation of the radioimmunoassay of circulating osteocalcin as a marker of bone remodeling.
1986 to 1991 : Staff scientist ('Chargé de Recherches') in INSERM Unit 234, "Pathologie des tissus calcifiés", Edouard Herriot hospital, Lyon, France, directed by Pr Pierre J Meunier. Development and validation of radioimmunoassays for SPARC/osteonectin - exploration of its intertissular variability and potential use as a marker.
1991 to 1993 : Visiting scientist in the "Medical Research Council Group in Periodontal Physiology", University of Toronto, Toronto, Ontario, Canada, working in Dr Jane E Aubin's laboratory. Study of the expression of bone related proteins during the differentiation of the osteoblast phenotype in in vitro models of osteogenesis.
1993 to 2003 : Staff scientist in INSERM Unit 403 "Physiopathologie des ostéopathies fragilisantes", Edouard Herriot Hospital, Lyon, France, directed by Pr Pierre D Delmas. Recruitement and differentiation of osteoprogenitors – regulation by matrix proteins and cytokines. In vitro models of osteogenesis.
Since 2004 : Staff scientist in LBTO-INSERM U1059, « Biologie Intégrative du Tissu Osseux », Faculté de Médecine, Université Jean Monnet, St Etienne, France, directed by Dr Laurence Vico.
My work focuses on the analysis of the functions of the SIBLING proteins BSP and osteopontin (OPN) in bone biology. In the the past years we have extensively characterized the phenotype of BSP knockout mice, and shown that it can be in part explained by the overexpression of OPN. We also showed that OPN can at least partly compensate for the absence of BSP, and that expression of either SIBLING is required for the anabolic action of PTH on bone. In order to unravel the functional specificty and redundancy of these two proteins, we have produced by genetic engineering mice with a double extinction of BSP and OPN (ANR "Mouse_Kosto" 2014-2017). Viable BSP-/- OPN-/- lines show non trivial chracteristics which lead to reinterpret single KO phenotypes. They are now being used to further analyse the interplay between SIBLING proteins.