Valerie URBACH PhD Cell and Molecular Physiology

Course and current status

After obtaining her PhD in 1993 at the University of Nice, France, she spent 4 years as a post-doctoral fellow at University College Cork funded by the Cystic Fibrosis Association of Ireland and by the French CF Association. In 1998, she obtained a Wellcome Trust Project grant on “the autocrine role of CFTR”. This work led on to the award of a Wellcome Trust Advanced Fellowship which allowed her to return to France, in Montpellier.

In 2003, she was successful for a permanent appointment as a researcher of the French National Institute of Health, INSERM, where she has continued to work in the area of CF and lung disease. She obtained funding for translational studies on the regulation of airway epithelial secretory functions. Using electrophysiology and advanced confocal microscopy techniques, her research has revealed novel effects of two endogenous specialized proresolving mediators, the lipoxin A4 and the resolvin D1 on airway epithelium function.

In 2010, Dr Urbach has obtained a 3 years leave-of-absence from INSERM to pursue this project at the National Children Research Centre (NCRC) at Crumlin Hospital in Dublin with an honorary lecturer appointment at the Royal College of Surgeons in Ireland.

Dr Urbach has now returned to France at the Mondor Institute for Biomedical Research (IMRB) in Paris where she is directing a research group focused on the abnormal bisosynthesis of specialized proresolving mediators in CF and its impact on CF airway disease.



Scientific summary

Biosynthesis and physiological impact of specialized proresolving mediators on the function of lung epithelium from children with cystic fibrosis. 

Cystic Fibrosis (CF) is the most common lethal genetic disease among Caucasians, and is characterized by progressive lung damage leading to early death. In healthy individuals, the body secretes a thin layer of fluid, which lines the airways and helps to fight infection by clearing mucus. The volume and composition of this fluid is tightly controlled. The gene mutation in CF leads to abnormal salt and water levels in this fluid, adversely affecting its protective functions. This leads to difficulty in clearing infection from the lungs with resultant infection and inflammation – the cause of lung damage over time.

Dr Urbach's team and other have shown that lipoxin A4, a member of the specialized proresolving mediator family that is normally synthetized in healthy lungs to fight inflammation was abnormally produced in the airways of individuals with CF, even in absence of bacterial or viral infection. Her current research program is based on the hypothesis that the specialized proresolving mediators (lipoxins, resolvins...) exert beneficial effects on airway epithelial functions through enhanced mucociliary clearance and epithelial repair. She is pursuing two main research axes : (i) the impact of the specialized proresolving mediators on major physiological functions controlled by the airway epithelium and which are altered in CF:  Cl- secretion,  Na+ absorption, ASL height, mucin and antimicrobial peptides production (ii) the impact of CFTR mutations on specialized proresolving mediators biosynthesis. These projects use a range of electrophysiological and advanced imaging technologies as well as molecular biology and interactomique approaches applied to CF and non-CF airway epithelial primary cultures grown from biopsies or nasal brushings, to human CF and non-CF bronchial epithelial cell lines and CF and non-CF mice.

This work has the potential to open up innovative therapy in CF.

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