CV Science

Véronique FREUND-MICHEL PhD in molecular and cellular Pharmacology, Pharm D

Course and current status

• Feb 2008 - until now : Lecturer in Pharmacology (permanent position), Laboratoire de Pharmacologie, INSERM U1045, UFR des Sciences Pharmaceutiques, Université Bordeaux Segalen, France

• Oct 2007 - jan 2008 : Research Associate, Respiratory Pharmacology Group, Airway disease section, Imperial College School of Medicine National Heart and Lung Institute, London, UK (Supervisor: Prof Maria Belvisi)

• Oct 2006 - sept 2007 : Post-doctoral training, Respiratory Pharmacology Group, Airway disease section, Imperial College School of Medicine National Heart and Lung Institute, London, UK (Supervisor: Prof Maria Belvisi) (European Respiratory Society long-term Research Fellowship Nr 154)

• 2002 - 2006 : PhD in Cellular and Molecular Pharmacology, Université Louis Pasteur-Strasbourg I, France (Supervisor: Dr Nelly Frossard)

• 2001 - 2002 : Master Degree in Pharmacology and Pharmacochemistry, Université Louis Pasteur-Strasbourg I, France

• 1997 - 2002 : Degree in Biological and Medical Sciences, Université Louis Pasteur-Strasbourg I, France

• 1995 - 2003 : Studies of Pharmacy, Option: Research, (PharmD degree obtained in October 2003), Faculty of Pharmacy, University Louis Pasteur-Strasbourg I,  France

Scientific summary

During my PhD, I investigated the potential role of the nerve growth factor NGF in asthma (Freund-Michel and Frossard, 2008). I showed that NGF is secreted by structural airway cells, in particular by the airway smooth muscle (Freund et al, 2002). I also showed that NGF induces airway smooth muscle proliferation through increased expression and activation of its TrkA receptor  (Freund-Michel et al, 2006 and 2008). My PhD results therefore suggest that NGF, whose expression is increased in asthmatic airways, may contribute to inflammation and airway remodeling in this disease.

Since I joined the Cardio-Thoracic Research Center of Bordeaux (INSERM U1045) in 2008, I have been investigating whether NGF may play a role in pulmonary hypertension. My results show NGF increased expression in pulmonary hypertension (in animal models and in humans), with NGF inducing pulmonary vascular inflammation and hyperreactivity ex vivo, as well as proliferation and migration of pulmonary vascular cells in vitro. I also showed that anti-NGF blocking antibodies prevent pulmonary hypertension in animal models in vivo, through prevention of pulmonary vascular inflammation,  hyperreactivity and remodeling. The precise mechanisms activated by NGF to induce these different effects are currently under investigation.