2010
DOI: 10.1177/0961203310361485
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The annexin A5-mediated pathogenic mechanism in the antiphospholipid syndrome: role in pregnancy losses and thrombosis

Abstract: Annexin A5 (AnxA5) binds to phospholipid bilayers, forming two-dimensional crystals that block the phospholipids from availability for coagulation enzyme reactions. Antiphospholipid (aPL) antibodies cause gaps in the ordered crystallization of AnxA5 which expose phospholipids and thereby accelerate blood coagulation reactions. The aPL antibody-mediated disruption of AnxA5 crystallization has been confirmed on artificial phospholipid bilayers and on cell membranes including endothelial cells, placental trophobl… Show more

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Cited by 128 publications
(88 citation statements)
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“…The pathophysiology of  2 -glycoprotein I was discussed by Matsuura (Matsuura E, et al 2010), the role of the receptor LRP8 by de Groot (de ) and involvement of protein C pathway by Urbanus (Urbanus RT, de Last B;2010). The annexin A5-mediated mechanism in pregnancy losses and thrombosis was clarified by Rand (Rand JH, et al 2010). These are the most important but definitely not all publications concerning antiphospholipid antibodies pathophysiology at this congress.…”
Section: Presencementioning
confidence: 99%
“…The pathophysiology of  2 -glycoprotein I was discussed by Matsuura (Matsuura E, et al 2010), the role of the receptor LRP8 by de Groot (de ) and involvement of protein C pathway by Urbanus (Urbanus RT, de Last B;2010). The annexin A5-mediated mechanism in pregnancy losses and thrombosis was clarified by Rand (Rand JH, et al 2010). These are the most important but definitely not all publications concerning antiphospholipid antibodies pathophysiology at this congress.…”
Section: Presencementioning
confidence: 99%
“…Antiphospholipid (aPL) antibodies cause gaps in the ordered crystallization of annexin A5, which expose phospholipids and thereby accelerate blood coagulation reactions. The reduction of annexinA5 levels on vascular cells may therefore be an important mechanisms leading to thrombosis and pregnancy loss in APS [67]. An ex vivostudy demonstratedthat plasmas with anti-ß2-GPI-dependent LAC that recognize domain I displayed significantly increased annexinA5 resistance.…”
Section: Fig (1) ß2-gp-i Interactions With Phospholipids and Antibomentioning
confidence: 99%
“…The main target antigens reported in patients with APS include beta-2-glycoprotein-1 ( 2GPI), prothrombin and annexin V (Galli et al, 2003). Other putative antigens are thrombin, protein C, protein S, thrombomodulin, tissue plasminogen activator, kininogens (high or low molecular), prekallikrein, factor VII/VIIa, factor XI, factor XII, complement component C4, heparan sulfate proteoglycan, heparin, oxidised low-density lipoproteins (Galli et al, 2003;Rand et al, 2010). The main autoantigens are attracted to negatively charged phospholipids exposed on the outer side of cell membranes in great amounts only under special circumstances such as damage or apoptosis (e.g.…”
Section: Pathogenetic Mechanisms Mediated By Apl 41 Vascular Thrombosismentioning
confidence: 99%