Endothelial Colony-Forming Cells from Idiopathic Pulmonary Fibrosis Patients Have a High Procoagulant Potential
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Endothelial Colony-Forming Cells from Idiopathic Pulmonary Fibrosis Patients Have a High Procoagulant Potential Paul Billoir 1,2 & Adeline Blandinières 1 & Nicolas Gendron 1 & Richard Chocron 3 & Sven Gunther 4 & Aurélien Philippe 1 & Coralie L. Guerin 5 & Dominique Israël-Biet 6 & David M. Smadja 1 Accepted: 10 September 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Idiopathic pulmonary fibrosis (IPF) is a severe, progressive and irreversible lung disease constantly associated with a major vascular remodeling process. Endothelial colony-forming cells (ECFCs) are human vasculogenic cells proposed as a cell therapy product or liquid biopsy in vascular disorders. Since the link between IPF and thrombosis has been largely proposed, the aim of our study was to explore hypercoagulability states in ECFCs from patients with IPF. We performed Thrombin generation assay (TGA) in cord blood (CB)-ECFCs, peripheral blood (PB)-ECFCs and IPF-ECFCs. Endogenous thrombin potential and peak were higher in IPF-ECFCs compared to CB-ECFCs and PB-ECFCs. As thrombin generation in ECFCs was increased, we evaluated anticoagulant proteins expressed on ECFCs membrane and identified thrombomodulin and EPCR. We found a significant decrease of both anticoagulant proteins at membrane using flow cytometry. This study is the first to examine ECFC thrombin generation in IPF. This new finding strongly argues for a role of ECFC in IPF pathophysiology and thrombotic related disorders in IPF. Keywords Endothelial progenitor . Endothelial colony forming cells . ECFCs . Idiopathic pulmonary fibrosis . EPCR . Thrombomodulin . Thrombin generation assay
Introduction Idiopathic pulmonary fibrosis (IPF) is a severe, progressive and irreversible lung disease. It mainly occurs in older adults and the prognosis is poor with a declining lung function, progressive dyspnea and a median survival after diagnosis comprised between 2 and 4 years
without treatment (1). Moreover, IPF lung parenchymal lesions are constantly associated with a major vascular remodeling process combining a rarefaction of vessels in fibrotic areas and their aberrant proliferation at the border of these areas (2, 3). It is associated with an imbalance between markers of endothelial activation and regeneration (4).
Electronic supplementary material The online version of this article (https://doi.org/10.1007/s12015-020-10043-4) contains supplementary material, which is available to authorized users. * David M. Smadja [email protected] 1
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Université de Paris, Innovative Therapies in Haemostasis, INSERM, 75006 Paris, AP-HP, Georges Pompidou European Hospital, F-75006 Paris, France, Service d’Hématologie et Laboratoire de Recherches Biochirugicales (Fondation Carpentier), 75015 Paris, France Normandie Univ, UNIROUEN, INSERM U1096, Rouen University Hospital, Vascular Hemostasis Unit, 76000 Rouen, France Université de Paris, PARCC, INSERM, 75015 Paris, France, AP-HP, Georges Pompidou European Hospital, Service d’accueil des urgences, 75015 Paris, Franc
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