Chantal M. Boulanger is a vascular biologist with internationally recognized expertise in extracellular vesicles. After receiveing her PhD (1986, University of Strasbourg), followed by postdoctoral trainings at the Mayo Clinic in Rochester and at the University Hospital Basel (1987-91), she was appointed Assistant Professor at Baylor College in Houston (1991-95) and Research Director at INSERM since 1995. She joined the Paris Cardiovascular Research Center in 2009. She has been leading an Inserm research team since 2004. Starting beginning of 2019, she has been appointed Director of the Paris Cardiovascular Research Center (PARCC) and co-director of the Physiopathology and cell biology department of the BioSPC Doctoral School at the University of Paris; she is also a member of the Scientific Council of INSERM. Chantal Boulanger authored over 200 publications (https://www.webofscience.com/wos/author/record/53072), 7 patents, 40 international conferences invited since 2009, and a MOOC Extracellular vesicles and cardiovascular diseases (ISEV 2019). The journal Circulation Research recognized her as an opinion leader in Cardiovascular Science (https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.117.311569).
Over the past twenty years, her team has been investigating extracellular vesicles as a biomarker of endothelial dysfunction and intercellular mediator during cardiovascular pathologies. Her current research aims to understand the mechanisms regulating the synthesis and the biological effects of extracellular vesicles in the cardiovascular context in order to develop biosynthetic vesicles mimicking the beneficial effects or inhibiting the deleterious effects of biological vesicles and thus to slow down the development cardiovascular pathologies. The latest awards she received are ATVB-AHA Special Recognition Award in Thrombosis (2014), the Lucie & Olga Fradiss Award from the French Society of Cardiology (2017) and the Jean-Paul Binet Award from the Fondation pour la Recherche Médicale (2019).
Until the late 1990’s my research was directed towards deciphering the mechanisms of endothelial dysfunction associated with the release of vasoactive factors such as nitric oxide, endothelin and arachidonic acid metabolites. In particular, I demonstrated the regulation of endothelin release by endothelial nitric oxide and by oxidized low-density lipoproteins. Since 2000, my group has been actively investigating two broad aspects of extracellular microparticles/microvesicles produced by endothelial cell activation, first their role as mediators of cell-cell communication in the vessel wall and second their potential as biomarkers of cardiovascular diseases.
In particular, we identified circulating microvesicles as the trigger for endothelial dysfunction in patients with coronary artery and related diseases. Subsequently, we showed that plasma microvesicles originating from injured endothelial cells provide a surrogate marker for endothelial dysfunction with prognostic value in patients with cardiovascular diseases. We identified microvesicles isolated from human atherosclerotic plaque as potent prothrombogenic mediators capable of recruiting monocytes to the endothelium following functional transfer of adhesion molecules. We also demonstrated the angiogenic effect of microvesicles resulting in plaque instability. We also identified a critical role of red-blood cell microvesicle in promoting endothelial injury in sickle cell disease and in myeloproliferative neoplasms. Recently we have extended our research on endothelial activation, induced by extracellular vesicles or other mechanisms, to include the potential role of endothelial autophagy in the development of atherosclerosis.
