VCBB Director, Associate Professor of Medicine, Pharmacology and Cancer Biology
I graduated in 2000 from Claude Bernard University in Lyon (France) with a PhD thesis focused on cell-extracellular matrix interactions. I trained as post-doctoral fellow in the laboratory of Dr. G. Karsenty at Baylor College of Medicine (Houston, TX), where I contributed to the characterization of the central and sympathetic nervous system as regulators of bone remodeling. During this period, I also had the opportunity to lead a project related to the skeletal complications seen in patients with neurofibromatosis type I (NF1), and to provide the first evidence for the role of neurofibromin in bone cells. It was also the time I met my wife, who made sure I’d stay in the US and who gave me confidence to transition to an independent scientist. In 2005, I took my first “real” job under the leadership of Dr. G. Mundy’s (UT Health Science Center, San Antonio), who introduced me to cancer and bone metastasis research. We moved in 2006 to Vanderbilt University (Nashville, TN) where I did not became a country music player or a gun owner but one of the core faculty of the new Vanderbilt Center for Bone Biology. Since then, I continued my research on NF1 and the role of the sympathetic nervous system on bone remodeling, and expanded my work to investigate early determinants of bone metastasis. I was promoted to the rank of Associate Professor on tenure in 2011 and took the direction of the Vanderbilt Center for Bone Biology, with the mission of facilitating multi-disciplinary and leading research in skeletal biology.
The two main areas of research in our laboratory are 1) the role of the central and peripheral sympathetic nervous system on bone remodeling and cancer metastasis and 2) the role of the RAS-GAP neurofibromin neurofibromin in skeleton development, growth, remodeling and repair.
The skeleton is an organ that is richly supplied with blood vessels but also nerves. These nerves can be sensory (hence the pain when you hurt your bones) but also sympathetic. The latter type regulates body involuntary functions such as heart rate or breathing. Several studies within the last 10 years revealed the role of these nerves in regulating the process that maintains the skeleton in an optimal state in adulthood, i.e. bone remodeling. Our efforts now focus in identifying the pathophysiological relevance of these findings, using genetic and pharmacologic approaches.
The second main interest of the laboratory relates to a condition called neurofibromatosis type I (NF1). Some patients with NF1 exhibit skeletal abnormalities, some of which can be associated with high morbidity and burden to the patient and family. Tibia bowing, fracture non-union and dystrophic scoliosis are the most problematic skeletal conditions and no satisfactory treatment is available. We use our expertise in bone physiology and bone cell biology to understand the etiology of these skeletal conditions and to propose pre-clinical mouse models as well as targeted therapeutic approaches aiming at preventing or curing such conditions.