Béatrice Hechler obtained her Ph.D. in Pharmacology at L. Pasteur University in Strasbourg in 1998. Her thesis focused on the identification and molecular and functional characterization of ADP platelet receptors, under the direction of Dr. Christian Gachet. From 1998 to 2000, she completed a postdoctoral fellowship at the Boston University School of Medicine, Whitaker Cardiovascular Institute, Boston, MA, USA, supervised by Prof. Katya Ravid. Then in 2000, she joined the INSERM U311 team in Strasbourg as a 2nd class INSERM researcher. CR1 INSERM since 2005, she is now project manager within the INSERM U1255 team.

Research Themes :

Three platelet receptors for nucleotides (ADP and ATP) contribute to platelet activation: two receptors coupled to ADP-activated G proteins: P2Y1 (identified in the laboratory) and P2Y12, (cloned in 2001 by different groups), and an ATP activated P2X1 ion channel (also identified by our team)

The P2Y12 receptor plays an essential role in the formation of arterial thromboses and is the molecular target of clopidogrel and prasugrel, among the most prescribed antiplatelet agents. Regarding P2X1 and P2Y1 receptors, our work on mice deficient for these receptors as well as the use of selective antagonists, allowed to characterize their function and their interest as targets for new antithrombotic drugs.

Aside from their role in platelet activation and arterial thrombosis, ADP and ATP have long been recognized as important players in inflammation. ATP is also a danger signal or DAMP “damage-associated molecular pattern” capable of recruiting and activating the cells of inflammation. The P2Y1 and P2X1 receptors are present on many cells involved in the inflammatory response, namely leukocytes (neutrophils, monocytes / macrophages), vascular endothelial cells (P2Y1) and smooth muscle cells (P2X1). We have shown that the endothelial cell P2Y1 receptor contributes to vascular inflammation by promoting leukocyte recruitment (Zerr, Hechler Circulation 2011) and the development of atherosclerotic lesions (Hechler, Circulation 2008). More recently, we seek to understand the roles of these P2 receptors in other processes where inflammation plays a major role in the development of various pathologies (sepsis, TRALI -transfusion-related acute lung injury- or acute respiratory distress syndrome). post-transfusion, venous thrombosis).

In addition, a central activity is the study of the cellular and molecular mechanisms of the formation of arterial thromboses. Among the approaches implanted in the laboratory, thrombosis models in small animals constitute a privileged axis. In recent years, we have developed various models of arterial thrombosis in mice, which have led to a better understanding of the mechanisms of platelet activation in contact with a breach of a healthy vascular wall: thrombosis by mechanical lesion, with using iron chloride or laser. On the other hand, the mechanisms involved in contact with an eroded or ruptured atheromatous plaque, which exposes to the circulating blood a heterogeneous material containing numerous platelet activators, are much less well known. Among these compounds, some are specifically expressed in atherosclerotic plaque and absent from healthy vessels, suggesting that the determinants of thrombosis formation will not be the same. Our goal is to identify the essential actors and activation pathways that are preferentially involved in the formation of atheromatous plaque thrombosis versus thrombosis in a healthy vessel. The most important actors could represent new pharmacological targets for effective and innovative antithrombotic therapeutics.


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