Increased soluble vascular cell adhesion molecule 1 concentrations in patients with primary or systemic lupus erythematosus-related antiphospholipid syndrome: Correlations with the severity of thrombosis

Kaplanski, Gilles; Cacoub, Patrice; Farnarier, Catherine; Marin, Valérie; Gregoire, R.; Gatel, A; Durand, J.M.; Harlé, Jean‐Robert; Bongrand, Pierre; Piette, Jean‐Charles

doi:10.1002/1529-0131(200001)43:1<55::aid-anr8>3.0.co;2-m

Cited by 110 publications

(68 citation statements)

References 34 publications

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“…32 Numerous reports have demonstrated that plasma from patients with the APS contains antibodies that bind and activate endothelial cells, 15,33 and that endothelial cell activation may occur in a ␤ 2 GPI-dependent manner. 17,22 The clinical relevance of endothelial cell activation in patients with the APS is supported by reports demonstrating increased circulating levels of tissue factor 34 and VCAM-1, 35 as well as endothelial microparticles, 36 in these individuals.…”

Section: Discussionsupporting

confidence: 93%

Annexin A2 mediates endothelial cell activation by antiphospholipid/anti-β2 glycoprotein I antibodies

Zhang

McCrae

2005

Blood

212

203

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Patients with antiphospholipid antibodies (APLAs) are at increased risk for arterial and venous thrombosis. Many APLAs associated with these events react with ␤ 2 glycoprotein I (␤ 2 GPI), and endothelial cell reactive antibodies that activate endothelial cells in a ␤ 2 GPI-dependent manner occur commonly in these patients. We previously reported that ␤ 2 GPI binds with high affinity to annexin A2 on the endothelial surface, though the relevance of this interaction to APLA/anti-␤ 2 GPI antibodyinduced endothelial activation has not been determined. In this report, we confirm that anti-␤ 2 GPI antibodies activate endothelial cells in the presence of ␤ 2 GPI, and demonstrate that anti-annexin A2 antibodies directly cause endothelial cell activation of a similar magnitude and with a similar time course. Moreover, bivalent anti-annexin A2 F(ab) 2 fragments also caused endothelial cell activation, whereas monomeric Fab fragments not only did not cause activation, but blocked activation induced by anti-annexin A2 antibodies and F(ab) 2 fragments, as well as that caused by anti-␤ 2 GPI antibodies in the presence of ␤ 2 GPI. These observations suggest a novel pathway for endothelial activation induced by APLA/anti-␤ 2 GPI antibodies that is initiated by crosslinking or clustering of annexin A2 on the endothelial surface. (Blood. 2005;105: 1964-1969

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Section: Discussionsupporting

confidence: 93%

Annexin A2 mediates endothelial cell activation by antiphospholipid/anti-β2 glycoprotein I antibodies

Zhang

McCrae

2005

Blood

212

203

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“…Once endothelial cells become activated, up-regulation of TF may be further augmented by a synergistic effect of TNF-a and factor Xa [37]. Other changes typical for this prothrombotic phenotype include increased expression of adhesion molecules (ICAM-1, VCAM-1, selectins E and P) [38,39], and formation of endothelial microparticles [40]. Raschi et al have shown that anti-beta 2 GPI antibodies induce translocation of NFjB in a manner similar to that elicited by LPS and TNF-a.…”

Section: Discussionmentioning

confidence: 99%

Increased level of tumor necrosis factor-α in patients with antiphospholipid syndrome: marker not only of inflammation but also of the prothrombotic state

2009

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“…Different indirect parameters of EC perturbation ex-vivo have been investigated with no definite conclusions. While some studies reported increased plasma levels of single soluble ADM or endothelial derived microparticles in APS patients, others did not confirm these findings [36][37][38][39]. Additional confounding variables-such as a concomitant associated immune-mediated systemic inflammatory disorder-did weaken the comparison.…”

Section: Do Apl Induce An Endothelial Perturbation In Vivo Too?mentioning

confidence: 99%

Inflammatory response and the endothelium

Meroni

Borghi

Raschi

et al. 2004

Thrombosis Research

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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 h2 glycoprotein I (h2GPI) 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.

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Increased soluble vascular cell adhesion molecule 1 concentrations in patients with primary or systemic lupus erythematosus-related antiphospholipid syndrome: Correlations with the severity of thrombosis

Abstract: Serum sVCAM-1 concentrations are increased in patients with primary APS, especially those with repeated thrombotic events or kidney involvement. These findings suggest that endothelial/ monocyte interaction may be important in the pathogenesis of primary APS.

Cited by 110 publications

References 34 publications

Annexin A2 mediates endothelial cell activation by antiphospholipid/anti-β2 glycoprotein I antibodies

Annexin A2 mediates endothelial cell activation by antiphospholipid/anti-β2 glycoprotein I antibodies

Increased level of tumor necrosis factor-α in patients with antiphospholipid syndrome: marker not only of inflammation but also of the prothrombotic state

Inflammatory response and the endothelium

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