The transport of high amounts of vascular endothelial growth factor by blood platelets underlines their potential contribution in systemic sclerosis angiogenesis

Anne Solanilla; Julien Villeneuve; Patrick Auguste; Michel Hugues; Ahmadou Alioum; Sébastien Lepreux; Jean-Pierre Ducroix; Pierre Duhaut; Claude Conri; Jean-François Viallard; Alan T. Nurden; Joël Constans; Jean Ripoche

doi:10.1093/rheumatology/kep154

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The transport of high amounts of vascular endothelial growth factor by blood platelets underlines their potential contribution in systemic sclerosis angiogenesis

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The transport of high amounts of vascular endothelial growth factor by blood platelets underlines their potential contribution in systemic sclerosis angiogenesis

Anne Solanilla, Julien Villeneuve, Patrick Auguste, Michel Hugues, Ahmadou Alioum, Sébastien Lepreux, Jean-Pierre Ducroix, Pierre Duhaut, Claude Conri, Jean-François Viallard, …

Rheumatology (Oxford, England), Vol.48(9), pp.1036-1044

01/09/2009

DOI: https://doi.org/10.1093/rheumatology/kep154

PMID: 19549789

Résumé

Blood platelets

Systemic sclerosis

Vascular endothelial growth factor

Objectives. Altered angiogenesis is a characteristic feature in SSc and remains ill-understood. VEGF is believed to play a central role. Serum VEGF is elevated in SSc patients but questions remain concerning the source of circulating VEGF. Here we investigated platelet activation and the role of platelets as a source of VEGF and other angiogenic mediators in this disease. Methods. A cohort of 40 patients with SSc was included. Age- and sex-matched healthy subjects and subjects presenting a primary RP were included as controls. Platelets were isolated, activated with thrombin and the secretion of VEGF, platelet derived growth factor, homodimeric form BB (PDGF-BB), TGF-β1 and angiopoietins-1 and -2 measured. Plasma concentrations of these mediators and the functionality of platelet-derived VEGF were also studied. Platelet activation was assayed by measuring plasma β-thromboglobulin and expression of P-selectin on platelets. The effect of iloprost on VEGF secretion by platelets was studied. Results. Platelets from SSc patients, in contrast to controls, secreted large amounts of VEGF when activated, but not PDGF-BB, TGF-β1 or angiopoietins. Increased expression of membrane P-selectin confirmed platelet activation in the patients. Iloprost inhibited VEGF secretion by platelets both in vivo and in vitro, through inhibition of platelet activation. Conclusions. Platelets transport high levels of VEGF in SSc. They may contribute to circulating VEGF because of ongoing activation in the course of the disease. If activated at the contact of injured endothelium, platelets may be important in the altered angiogenesis associated with the disease through the secretion of high levels of VEGF.

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Titre: The transport of high amounts of vascular endothelial growth factor by blood platelets underlines their potential contribution in systemic sclerosis angiogenesis
Créateurs - sans rôle: Anne Solanilla - Inserm U 889, IFR 66, ISPED, Bordeaux University, Bordeaux, Internal Medicine Department, Amiens University Hospital, Amiens, Internal and Vascular Medicine Department, Internal Medicine Department A and Platelet Diseases Reference Centre, IFR 4, Bordeaux University Hospital, Bordeaux, France
Julien Villeneuve - Inserm U 889, IFR 66, ISPED, Bordeaux University, Bordeaux, Internal Medicine Department, Amiens University Hospital, Amiens, Internal and Vascular Medicine Department, Internal Medicine Department A and Platelet Diseases Reference Centre, IFR 4, Bordeaux University Hospital, Bordeaux, France
Patrick Auguste - Inserm U 889, IFR 66, ISPED, Bordeaux University, Bordeaux, Internal Medicine Department, Amiens University Hospital, Amiens, Internal and Vascular Medicine Department, Internal Medicine Department A and Platelet Diseases Reference Centre, IFR 4, Bordeaux University Hospital, Bordeaux, France
Michel Hugues - Inserm U 889, IFR 66, ISPED, Bordeaux University, Bordeaux, Internal Medicine Department, Amiens University Hospital, Amiens, Internal and Vascular Medicine Department, Internal Medicine Department A and Platelet Diseases Reference Centre, IFR 4, Bordeaux University Hospital, Bordeaux, France
Ahmadou Alioum - Inserm U 889, IFR 66, ISPED, Bordeaux University, Bordeaux, Internal Medicine Department, Amiens University Hospital, Amiens, Internal and Vascular Medicine Department, Internal Medicine Department A and Platelet Diseases Reference Centre, IFR 4, Bordeaux University Hospital, Bordeaux, France
Sébastien Lepreux - Inserm U 889, IFR 66, ISPED, Bordeaux University, Bordeaux, Internal Medicine Department, Amiens University Hospital, Amiens, Internal and Vascular Medicine Department, Internal Medicine Department A and Platelet Diseases Reference Centre, IFR 4, Bordeaux University Hospital, Bordeaux, France
Jean-Pierre Ducroix - Inserm U 889, IFR 66, ISPED, Bordeaux University, Bordeaux, Internal Medicine Department, Amiens University Hospital, Amiens, Internal and Vascular Medicine Department, Internal Medicine Department A and Platelet Diseases Reference Centre, IFR 4, Bordeaux University Hospital, Bordeaux, France
Pierre Duhaut - Inserm U 889, IFR 66, ISPED, Bordeaux University, Bordeaux, Internal Medicine Department, Amiens University Hospital, Amiens, Internal and Vascular Medicine Department, Internal Medicine Department A and Platelet Diseases Reference Centre, IFR 4, Bordeaux University Hospital, Bordeaux, France
Claude Conri - Inserm U 889, IFR 66, ISPED, Bordeaux University, Bordeaux, Internal Medicine Department, Amiens University Hospital, Amiens, Internal and Vascular Medicine Department, Internal Medicine Department A and Platelet Diseases Reference Centre, IFR 4, Bordeaux University Hospital, Bordeaux, France
Jean-François Viallard - Inserm U 889, IFR 66, ISPED, Bordeaux University, Bordeaux, Internal Medicine Department, Amiens University Hospital, Amiens, Internal and Vascular Medicine Department, Internal Medicine Department A and Platelet Diseases Reference Centre, IFR 4, Bordeaux University Hospital, Bordeaux, France
Alan T. Nurden - Inserm U 889, IFR 66, ISPED, Bordeaux University, Bordeaux, Internal Medicine Department, Amiens University Hospital, Amiens, Internal and Vascular Medicine Department, Internal Medicine Department A and Platelet Diseases Reference Centre, IFR 4, Bordeaux University Hospital, Bordeaux, France
Joël Constans - Inserm U 889, IFR 66, ISPED, Bordeaux University, Bordeaux, Internal Medicine Department, Amiens University Hospital, Amiens, Internal and Vascular Medicine Department, Internal Medicine Department A and Platelet Diseases Reference Centre, IFR 4, Bordeaux University Hospital, Bordeaux, France
Jean Ripoche - Inserm U 889, IFR 66, ISPED, Bordeaux University, Bordeaux, Internal Medicine Department, Amiens University Hospital, Amiens, Internal and Vascular Medicine Department, Internal Medicine Department A and Platelet Diseases Reference Centre, IFR 4, Bordeaux University Hospital, Bordeaux, France
Détails de publication: Rheumatology (Oxford, England), Vol.48(9), pp.1036-1044
Éditeur: Oxford University Press
Nombre de pages: 9
Identifiants: 99163012909311
Unité académique: Institut de Génomique Fonctionnelle - IGF
Langue: English
Type de ressource: Journal article