Christophe GUIGNABERT
  • E-mail :[email]
  • Phone : +33 1 40 94 88 33
  • Location : Le Plessis-Robinson, France
Last update 2017-12-02 14:59:20.924

Christophe GUIGNABERT PhD Cardiovascular Research

Course and current status

Dr. Christophe GUIGNABERT is a Research Director (DR2) at Inserm (Associate Professor). Since 2010, he is leading a research team entitled « Cellular and Molecular bases of Pulmonary Endothelial Dysfunction in PAH » in the Inserm research unit 999. His research team is currently composed of 1 assitant professor (CR1 INSERM), 3 engineers, 1 technician, 2 post-doc, 2 Ph.D and 1 Master students.

Current Research and Scholarly Interests: http://www.u999.u-psud.fr/en/unit-u999/research-topics/pah-physiology-topics.html

-Since 2017:  Associate Professor (Director of Research (DR2) INSERM, Ph.D) - INSERM UMR_S 999 - Univ Paris-Sud - Université Paris-Saclay Pr. Marc Humbert's lab

-2012-2017:  Assistant Professor (Chargé de Recherche (CR1) INSERM, Ph.D) - INSERM UMR_S 999 - Univ Paris-Sud - Université Paris-Saclay Pr. Marc Humbert's lab

-2012: Accreditation to conduct research (HDR)                                                      

-2010-2012:  Assistant Professor (Chargé de Recherche (CR2) INSERM) - INSERM UMR_S 999 - Univ Paris-Sud - Université Paris-SaclayPr. Marc Humbert's lab

-2008-2010:  Post-Doct #3 (Universite Paris-Sud - Le Kremlin Bicêtre, France) - INSERM UMR_S 999 - Univ Paris-Sud - Université Paris-Saclay Pr. Marc Humbert's lab

-2006-2008:  Post-Doct #2 (STANFORD University, CA, USA) - Stanford University School of Medicine - Pr. Marlene Rabinovitch's lab

-2004-2006:  Post-Doct #1 (Univ. Paris-Est Créteil - Val de Marne, France) - INSERM UMR_S 651 - Univ. Paris-Est Créteil - Pr. Serge Adnot's Lab

-2001-2005:  Ph.D "Epithelial alveolar repair & MECs & MMPs" - Univ. Paris-Est Créteil - Val de Marne, France - Pr. Marie-Pia d'Ortho's lab

Scientific summary

My primary research for the past several years seeks to: (1) Provide a better understanding of the role played by ECs in pulmonary vascular remodeling; (2) Investigate abnormalities in EC communications with other vascular cells (smooth muscle cells, myofibroblasts and pericytes) and immune cells (Treg); (3) Restore the expression/protein activity identified in vitro on isolated cells and in vivo through experimental models of pulmonary hypertension. 

My research group has already been able to highlight several events reflecting major functional alterations in the pulmonary vascular endothelium, including among others: 1) a transition from a quiescent state (without adhesion capacity) to an activated state with adhesive capacity (Le Hiress et al. Am J Respir Crit Care Med 2015); 2) an aberrant hyper-proliferative and apoptosis resistant phenotype (Tu et al. Am J Respir Cell Mol Biol. 2011)3) a pro-inflammatory phenotype characterized by an excessive release of various key cytokines and chemokines: interleukin (IL)-1α, IL-6, IL-8, IL-12, CCL2/monocyte chemotactic protein (MCP)-1 (Ricard et al. Circulation 2014 ; Le Hiress et al. Am J Respir Crit Care Med 2015); 4) an excessive production and secretion of various key growth factors including fibroblast growth factor-2 (FGF-2; basic FGF), angiotensin-II (Ang II), macrophage migration inhibitory factor (MIF) and leptin (Tu et al. Am J Respir Cell Mol Biol. 2011; Tu et al. Am J Respir Crit Care Med 2012; Ricard et al. Circulation 2014; de Man et al. Am J Respir Crit Care. Med 2012; Huertas et al. Eur Respir J. 2012; Huertas, et al. Eur Respir J. 2015; Le Hiress et al. Am J Respir Crit Care Med 2015; Huertas et al. Chest 2016)

The underlying mechanisms remain unknown and substantial work remains to be done. Our research interests focuses on the mechanisms by which pulmonary ECs interact with their environment. Firstly, we are studying the importance of the MIF/CD74 signaling pathway at the crossroad of Inflammation and Endothelial dysfunction (ANR jeune chercheur 'EPINE'). Secondly, we are exploring the endothelium/ pericyte interactions as well as the endothelial/ immune cell interactions (with regulatory T cells (Tregs) in particular) (Equipe FRM label 2015 of the Fondation Recherche Médicale). Finally, we are studying the mechanisms of certain iatrogenic agents, such as drugs, on endothelial dysfunction (project ANSM 'VIGIAPATH').

Scientific Focus: Pulmonary hypertension (PH) – Pulmonary vascular remodeling – Endothelial dysfunction – Endothelial communications – Pericyte – Endothelial cell – Growth factors – Animal models.

Website: http://www.u999.u-psud.fr/en/unit-u999/research-topics/team-1-research-topics/pah-physiology-topics.html

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