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Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Res+Pract+Thromb+Haemost 2018 ; 2 (2): 380-9 Nephropedia Template TP
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Effects of anti??2GPI antibodies on VWF release from human umbilical vein endothelial cells and ADAMTS13 activity #MMPMID30046742
Ng CJ; McCrae KR; Ashworth K; Sosa LJ; Betapudi V; Manco?Johnson MJ; Liu A; Dong J; Chung D; White?Adams TC; López JA; Di Paola J
Res Pract Thromb Haemost 2018[Apr]; 2 (2): 380-9 PMID30046742show ga
Essentials: The antiphospholipid syndrome predisposes to thrombosis due to activation of endothelium and blood components.The role of anti??2GPI antibodies in VWF release and ADAMTS13 function is not well understood.Some anti??2GPI antibodies induce endothelial release of soluble VWF but not VWF strings.An anti??2GPI antibody can decrease ADAMTS13 activity in vitro similar to ex vivo results. Background: Antiphospholipid syndrome (APS) is characterized by recurrent thromboembolic events in the setting of pathologic autoantibodies, some of which are directed to ?2?Glycoprotein 1 (?2GPI). The mechanisms of thrombosis in APS appear to be multifactorial and likely include a component of endothelial activation. Among other things, activated endothelium secretes von Willebrand factor, a hemostatic protein that in excess can increase the risk of thrombosis. Objective: We hypothesized that anti??2GPI antibodies could regulate the release and modulation of VWF from endothelial cells. Patients/Methods: Isolated anti??2GPI antibodies from patients with APS were assayed for their ability to induced VWF release from HUVECs and modulate the effects of ADAMTS13 in a shear?dependent assay. Results: We observed that anti??2GPI antibodies from some patients with APS induced VWF release from human endothelial cells but did not induce formation of cell?anchored VWF?platelet strings. Finally, we also determined that one of the Anti??2GPI antibodies tested can inhibit the function of ADAMTS13, the main modulator of extracellular VWF. Conclusions: These results suggest that VWF and ADAMTS13 may play a role in the prothrombotic phenotype of APS.