Géraldine Vitry

2019 Paroian Family PH Research Scholarship

Pulmonary Hypertension Research Group, Centre de recherche de l’Institut universitaire de cardiologie et de pneumologie de Québec, Laval University, Québec City, QC

Under the supervision of: Dr. Roxane Paulin

About Géraldine Vitry 

Vitry obtained a degree in Life Sciences in Cellular Biology and Physiology and a master’s degree in Therapies and Technologies with a special mention from the University of Paris 13 in France. In this context, she had the opportunity to work on the cystic development of the kidney in Renal Cyst and Diabetes (RCAD) pathology during a two-month internship, then to study telomeres and their potential as a therapeutic target in cancers for seven months. These experiences confirmed her passion for research. 

In 2016, she enthusiastically joined the Québec pulmonary hypertension research group, led by Drs. Sébastien Bonnet and Steeve Provencher, to study the molecular and cellular mechanisms involved in the pathogenesis of pulmonary arterial hypertension. She is completing her doctorate at Laval University under the supervision of Dr. Roxane Paulin.

Project:

Involvement of NUDIX proteins in the pathogenesis of pulmonary arterial hypertension

Involvement of NUDIX proteins in the pathogenesis of pulmonary arterial hypertension Pulmonary hypertension is characterized by high blood pressure in the pulmonary arteries due to obstruction of these vessels (imagine closing your fist on an inflated balloon).The heartmust then putmore effort intomoving the blood in the bloodstreamand in ensuring the oxygenation of all tissues in the body. Patients with PAH die of heart failure in less than 5 years if left untreated.We must therefore improve our understanding of the disease in order to develop better treatments.

The cells that make up the wall of the small pulmonary arteries of PAH patients, the PAH CMLAPs, survive and proliferate abnormally despite hostile conditions (hypoxia, inflammation, mechanical stress), causing their accumulation and contributing to the progressive obstruction of these vessels. This suggests that they have acquired molecular mechanisms to adapt, strongly reminiscent of the characteristics of cancer cells. The loss of these mechanisms should make these cells vulnerable and lead to their death. We have identified NUDIX proteins as a potential shield for CMLAP-HTAP because they are involved in DNA protection and metabolism optimization (availability and mobilization of energy resources).

Our project aims to highlight the role of NUDIX proteins in the survival of pulmonary artery cells and to evaluate the therapeutic potential of their inhibition by (S)-Crizotinib (already in clinical study in cancer) in different animalmodels of PAH and cell lines from PAH patients. This study examines a new therapeutic strategy for patients and will improve our understanding of the disease at the cellular and molecular levels.