Christophe Guignabert

Inserm, France 0000-0002-8545-4452

RESEARCH SCIENTIST - PhD - Group leader, CR INSERM - SCIENTIFIC FOCUS: Pulmonary hypertension (PH); Pulmonary vascular remodeling; Endothelial dysfunction; Endothelial communications; Pericyte; Endothelial cell; Growth factors; Animal models. - CURRENT RESEARCH INTERESTS: My primary research for the past several years seeks to (1) provide a better understanding of the role played by the pulmonary-endothelial cells (ECs) in idiopathic PH (iPH), (2) improve our knowledge on the endothelial communication with other cells that modulate their (dys)function, (3) and to identify target genes potentially involved in the modulation of endothelial dysfunction. We observed evidence for paracrine overproduction of serotonin, endothelin-1, and FGF2 specifically by human ECs from iPH patients that contribute to the increased smooth muscle cell proliferation. During my postdoctoral research, I have found that only a selective alteration of ECs resulting in disruption of the endothelial peroxisome proliferators activated receptor (PPAR) gamma signaling in mice is sufficient to cause mild PH and impair recovery from chronic hypoxia-induced PH. Moreover, our recent results have revealed that cultured ECs from iPH patients present phenotypic abnormalities including a higher growth response to growth factors and apoptosis resistance. Although our observations support the hypothesis that pulmonary ECs play a central role in the maintenance of vascular structure and that endothelial dysfunction is a major participant in the pathogenesis of PH, their exact contributions to the disease remain unknown. -

Biography Updated on 16 April 2013

Scholarly Contributions [Data Provided by scopus]