2012-Present Research assistant (Inserm permanent position as 'CR1') in M. Cogné's team, UMR CNRS 7276 (Director : M. Cogné), Limoges University, Limoges, France
2006-2012 Research assistant (Inserm permanent position as 'CR1') in F. Terzi's team, Inserm U845 (Director : P. Kelly/G. Friedlander), Paris Descartes University - Necker site, Paris, France
2000-2006 Research assistant (Inserm permanent position as 'CR2') in M. Pretolani's team, Inserm U408/U700 (Director : M. Aubier/M. Pretolani), Paris Diderot University - Bichat site, Paris, France
1998-2000 Post doctoral fellow in E.S. Alnemri's team, Kimmel Cancer Institute (Director : C. Croce), Thomas Jefferson University, Philadelphia, USA
1994-1998 M2 (ex-DEA) then PhD student in M. Pretolani's team, Inserm U285/U485 (Director : B.B. Vargaftif), Pasteur Institute, Paris - PhD degree from Pierre and Marie Curie University, Paris, France
Before 1994 Bachelor's degree in Biotechnology, Blaise Pascal University, Clermont-Ferrand, France, then Master's degree in Cell Biology and Animal Physiology, Montpellier 2 University, Montpellier, France
Born in 1970
Many diseases are characterized by modifications of tissue architecture, also known as tissue remodeling. For instance, a main feature of severe asthma is the irreversible thickening of the bronchial wall. In other organs such as kidney, remodeling translates into cysts and fibrosis. Changes in tissue architecture are often positively correlated wih the severity of diseases. Thus, unveiling the phenomena, the cells and the molecules that are involved in tissue remodeling is a prerequisite for the development of innovative therapeutics.
All the work I have done so far focused on tissue remodeling and on the phenomena whose deregulation contributes to alterations of organ architecture. These phenomena include 1) inflammation, and 2) migration, proliferation, survival, changes of morphology (size, shape), differentiation, and death of structural cells (epithelial cells, fibroblasts,...).
More specifically, using primary cell cultures and mouse models, I have studied how : 1) a defect in the apoptosis of the eosinophil leucocyte contributes to cell accumulation and to bronchial wall remodeling in asthma (PhD), 2) apoptotic and inflammatory caspases are activated (post doc), 3) nuclear receptors (retinoic acid receptors and PPARs) participate in the alteration of airways wall architecture (CR2), and 4) the seven ligands of EGFR are differentially involved in the changes of kidney structure during acute injury and chronic nephropathies (CR1). I’m presently evaluating the role of neutrophil leucocytes and of IgA anomalies in kidney structural lesions during IgA nephropathy.
Key words : inflammation, epithelial cells, lung, kidney, apoptosis, cell biology, murine models