• E-mail :[email]
  • Phone : +33 1 40 25 86 03
  • Location : PARIS, France
Last update 2016-09-07 11:52:07.298

Benoît Ho-Tin-Noé PhD Pathophysiology and Cell Biology

Course and current status

2009-present                Full-time researcher at INSERM Unit 698/1148, Bichat Hospital, Paris, France.

2006-2008                      Postdoctoral fellow at The Wagner Lab, Immune Disease Institute, Department of Pathology, Harvard Medical School, Boston, MA, USA.

2002-2005                                            PhD Pathophysiology and Cell Biology at INSERM Unit 698 “Cardiovascular Remodeling”,

Université Paris VII Denis Diderot, Paris, FRANCE.

1999-2002                                         Master of Science (Summa cum Laude), Vascular Cell Biology and Physiology, Université Paris VII Denis Diderot, Paris, FRANCE.

1997-1999                      Bachelor of Science (Cum Laude), Cell Biology, Université Paris VII Denis Diderot, Paris, FRANCE.

Scientific summary

During my PhD (October 2002- December 2005), I studied the mechanisms of pericellular proteolysis and its deleterious consequences on cell adhesion, organisation and survival. Our hypothesis was that plasmin-mediated extracellular proteolysis could play a role in the induction of smooth muscle cell apoptosis, a phenomenon that contributes to the evolution of aneurysms and to the destabilization of atherosclerotic plaques.

In February 2006, I joined The Wagner Lab (Immune Disease Institute, Department of Pathology, Harvard Medical School) that is specialized in intravital microscopy techniques applied to the study of thrombosis and inflammation in mice. My postdoctoral project consisted in investigating the role of platelets in the regulation of vascular integrity at sites of acute leukocyte recruitment and in tumors, in which the cellular and molecular mediators of inflammation are also thought to play a role.

I got a tenure position as a full time researcher at INSERM Unit 698 in February 2009. While pursuing studying the vasculoprotective role of platelets, I have started to investigate the mechanisms that could contribute to promote intraplaque hemorrhage and plaque destabilization, with special emphasis on atheroma-associated neoangiogenesis and cholesterol crystallization. Our ongoing studies point toward a crucial role for smooth muscle cells in initiating both phenomena in the early stages of the atherothrombotic disease.

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