Antiphospholipid-mediated endothelium perturbation plays a role in antiphospholipid syndrome (APS)-associated vasculopathy. Antiphospholipid antibodies activate endothelium both in vitro and in vivo experimental models by inducing a pro-inflammatory/-coagulant phenotype; the antibodies recognize β2 glycoprotein I (β2GPI) on human endothelial cells (EC) from different parts of the vasculature. In spite of such large in vitro evidence, few studies have addressed the issue whether or not a comparable endothelial perturbation might be detectable in vivo. We investigated several indirect ex vivo parameters of endothelial dysfunction: plasma levels of soluble adhesion molecules (sADM), soluble thrombomodulin (sTM), von Willebrand factor (vWF) and tissue plasminogen activator (t-PA) by solid-phase assays. The study included: patients with primary antiphospholipid syndrome (n=32), with the syndrome secondary to non-active systemic lupus erythematosus (SLE, n=10), six patients with persistent antiphospholipid positivity at medium/high titre without any clinical manifestation of the syndrome. Fifty-two age and sex matched healthy subjects have been enrolled as controls. In addition, circulating endothelial cells identified by flow cytometry and the brachial artery flow-mediated vasodilation (FMV) were evaluated in 26 patients (20 primary and 6 lupus syndromes) and 30 healthy controls. Plasma levels of soluble adhesion molecules did not differ from controls, while a significant increase in von Willebrand factor titres (P<0.05) was found. No significant difference was found regarding the number of circulating endothelial cells and flow-mediated vasodilation. As a whole, these findings do suggest that antiphospholipid antibodies per se are not able to support a full-blown endothelial perturbation in vivo. As shown in antiphospholipid syndrome experimental animal models, a two-hit hypothesis is suggested. © 2004 Elsevier Ltd. All rights reserved
Meroni, P., Borghi, M., Raschi, E., Ventura, D., Sarzi Puttini, P., Atzeni, F., et al. (2004). Inflammatory response and the endothelium. THROMBOSIS RESEARCH, 114(5-6 SPEC. ISS.), 329-334 [10.1016/j.thromres.2004.06.045].
Citazione: | Meroni, P., Borghi, M., Raschi, E., Ventura, D., Sarzi Puttini, P., Atzeni, F., et al. (2004). Inflammatory response and the endothelium. THROMBOSIS RESEARCH, 114(5-6 SPEC. ISS.), 329-334 [10.1016/j.thromres.2004.06.045]. | |
Tipo: | Articolo in rivista - Review Essay | |
Carattere della pubblicazione: | Scientifica | |
Presenza di un coautore afferente ad Istituzioni straniere: | No | |
Titolo: | Inflammatory response and the endothelium | |
Autori: | Meroni, P; Borghi, M; Raschi, E; Ventura, D; Sarzi Puttini, P; Atzeni, F; Lonati, L; Parati, G; Tincani, A; Mari, D; Tedesco, F | |
Autori: | ||
Data di pubblicazione: | 2004 | |
Lingua: | English | |
Rivista: | THROMBOSIS RESEARCH | |
Digital Object Identifier (DOI): | http://dx.doi.org/10.1016/j.thromres.2004.06.045 | |
Appare nelle tipologie: | 01 - Articolo su rivista |