Annexin A2 is involved in antiphospholipid antibody-mediated pathogenic effects in vitro and in vivo

Romay-Penabad, Zurina; Montiel-Manzano, Maria Guadalupe; Shilagard, Tuya; Papalardo, Elizabeth; Vargas, Gracie; Deora, Arun B.; Wang, Michael; Jacovina, Andrew T.; Garcı́a-Latorre, Ethel; Reyes‐Maldonado, Elba; Hajjar, Katherine A.; Pierangeli, Silvia S.

doi:10.1182/blood-2008-11-188698

Cited by 128 publications

(106 citation statements)

References 59 publications

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“…Furthermore, anti-annexin A2 antibodies isolated from plasma of patients are equally efficient as anti-β2GP1 antibodies to induce TF expression by EC [69]. Antiannexin A2 antibodies increased also thrombosis extent in a mouse model of thrombosis [30]. These results suggest that EC activation trigger by anti-β2GP1 or anti-annexin A2 antibodies induce a cross-linking or clustering of annexin A2/β2GP1 complexes at the cell surface sufficient to trigger EC activation.…”

Section: Annexin A2 As An Accessory Protein For Aplamentioning

confidence: 82%

“…Several candidate receptors have been proposed for aPLA: in vivo studies have shown that deficiencies of TLR4 [29], Annexin A2 [30], ApoER2 [31] and several complement factors [20] reduced the pathogenic effects of aPLA. Moreover, ex vivo studies suggest a role for TLR2 [32][33][34], CD14 [34], GPIbα [35] and TLR8 [36] in aPLA-activated monocytes and EC.…”

Section: Candidate Receptors For Aplamentioning

confidence: 99%

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Receptors involved in cell activation by antiphospholipid antibodies

Brandt

Kruithof

Moerloose

2013

Thrombosis Research

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The antiphospholipid syndrome (APS) is an autoimmune disease associated with arterial or venous thrombosis and/or recurrent fetal loss and is caused by pathogenic antiphospholipid antibodies (aPLA). The plasma protein β2-glycoprotein 1 (β2GP1) has been identified as a major target of aPLA associated with APS. Cell activation by aPLA appears to be a major pathogenic cause in the pathogenesis of APS. Receptors, co-receptors and accessory molecules are known to assist the pathogenic effects of aPLA. Members of the TLR family and the platelet receptor apolipoprotein E receptor 2' (apoER2'), a receptor belonging to the low-density lipoprotein receptor (LDL-R) family, as well as GPIbα, were identified as putative candidates for aPLA recognition. CD14, a co-receptor for TLR2 and TLR4, and annexin A2, a ubiquitous Ca2+ -binding protein that is essential for actin-dependent vesicle transport, could serve as important accessory molecules in mediating the pathogenic effects of aPLA. Finally, complement activation has been reported in association with the pathogenicity of APS. The relative contribution of these different mechanisms in the pathogenesis of APS is controversial. Here, we review the various in vivo and in vitro models that have been used to investigate the pathogenic mechanisms of aPLA in APS

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Section: Annexin A2 As An Accessory Protein For Aplamentioning

confidence: 82%

Section: Candidate Receptors For Aplamentioning

confidence: 99%

Receptors involved in cell activation by antiphospholipid antibodies

Brandt

Kruithof

Moerloose

2013

Thrombosis Research

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“…Further work is needed to define how antibodies penetrate into the cell [58] Once antibodies from patients with APS enter monocytes and endothelial cells, they can disrupt mitochondrial function, leading to the generation of ROS and the subsequent expression of TF [59]. Studies in animal models have demonstrated that annexin A2 knockout mice [60] and apoE receptor knockout mice [61] are protected from associated thrombosis with aPL. It is known that A1, an analogue of apoE R2 inhibits ß2-GPI antibodies effects in vivo and in vitro [62,63].…”

Section: Fig (1) ß2-gp-i Interactions With Phospholipids and Antibomentioning

confidence: 99%

The Pathophysiology of Antiphospholipid Syndrome

Sada¹,

Cohen²,

Isenberg³

2015

TOUNJ

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“…Pierangeli et al In summary, these animal models of thrombosis and endothelial cell activation have not only been useful in demonstrating the pathogenic effects of aPL antibodies and their causative role in inducing APS morbidity, but have also been instrumental in dissecting the intracellular mechanisms involved, in identifying cellular receptors activated by aPL antibodies in vivo and in testing potential new treatments for APS (discussed in detail in other sections of this chapter) [37,39,51,[93][94][95][96][97][98][99][100][101][102][103][104][105].…”

Section: A Animal Models Of Thrombosis and Endothelial Cell Activationmentioning

confidence: 99%