TEAM LEADER : Chantal BOULANGER
Mail : chantal.boulanger@inserm.fr
PHONE :+33 1 53 98 80 86
Localisation : Room 220
Doctoral School: Ecole Doctorale Bio-Sorbonne Paris Cité (ED 562), Department of Cellular and Molecular Biology, Physiology and Pathology
Our overall objective is to understand the potential role of extracellular vesicles (EVs) as surrogate markers of disease development and as new mediator of vascular injury and repair. EVs stemming from cellular membrane can signal to neighboring cells and influence disease progression or repair mechanisms. They also present an attractive potential as a new plasma marker to stratify cardiovascular risk. In addition, plasma EVs isolated from patients with vascular diseases can transfer their cargos to endothelial cells, and contribute to vascular dysregulation. We also further characterized EVs to better understand their role in cell-cell communication, in particular in the heart after myocardial infarction where they stimulate infiltrating monocytes, therefore contributing to the repair response in ischemic diseases.
We aim to understand how EVs of endothelial and cardiomyocyte origin regulate intra-cardiac and remote inflammatory responses after myocardial infarction and in diabetes, and in particular the role of non-coding RNA transfer to target cells. Our objectives are to better characterize the protein and non-coding RNA cargos of cardiomyocyte-derived EVs, track them into the circulation and identify their biodistribution in vivo in order to understand how EVs regulate the inflammatory process after myocardial infarction.
Diseases associated with intravascular hemolysis, such as sickle cell disease, are characterized by dysfunctional plasma annexins, resulting in abnormal EV numbers and composition, with increased procoagulant activity. Our objectives are to determine the molecular determinants of annexin inhibition during hemolysis, better understand the pathophysiological significance of EVs, and develop new EV inhibitors with our industrial and academic partners.
Our current objectives are a) to explore how endothelial autophagy affects EV release, composition and fate in atheroprone areas of the vasculature and b) to test the hypothesis that stimulation of autophagic flux may constitute an attractive therapeutic strategy in atherosclerosis.
