In vitro effect of anti-β2 glycoprotein I antibodies on P-selectin expression, a marker of platelet activation

• Main Authors: A. Hoxha (Author), M. Tonello (Author), E. Falcinelli (Author), S Giannini (Author), A. Ruffatti (Author), A. Bontadi (Author), P. Gresele (Author), L. Punzi (Author)
• Format: Book
• Published: PAGEPress Publications, 2012-03-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.
• Notes: 10.4081/reumatismo.2012.35; 0048-7449; 2240-2683
• Keywords: Anti-β2Glicoprotein I antibodies, P-selectin, Platelet activation, Antiphospholipid syndrome; Medicine; R; Internal medicine; RC31-1245
• Source: Reumatismo, Vol 64, Iss 1, Pp 35-39 (2012)

Antiphospholipid antibodies (aPL) associated with thromboembolic events and/or pregnancy morbidity characterize the so-called antiphospholipid syndrome (APS). Beta2glycoprotein I (β2GPI) is the main target antigen for aPL, but the pathogenic role of anti-β2GPI antibodies (aβ2GPI) is still unclear. Some authors assume they play a role in activating platelets. We evaluated the effects of aβ2GPI antibodies on platelet P-selectin expression. Aβ2GPI antibodies in the plasma of a pregnant APS patient were isolated by affinity chromatography at two different stages (catastrophic and quiescent) of the disease. Gel filtered platelets (100 x 109/L) from healthy volunteers were incubated with β2-GPI (20 µg/mL) and with different concentrations (5. 25 and 50 µg/mL) of aβ2GPI antibodies. P-selectin surface expression on platelets was assessed by flow cytometry using a specific fluorescent antibody directed against P-selectin. Aβ2GPI antibodies induced platelet activation only in the presence of thrombin receptor activator for peptide 6 (TRAP-6), a platelet agonist, at a subthreshold concentration. Aβ2GPI antibody enhancement on platelet surface P-selectin expression was stronger in the catastrophic than in the quiescent phase of the disease (47 vs 15%). TRAP-6 dependent platelet activation by aβ2GPI antibodies is consistent with the "two hit" pathogenetic hypothesis for thrombosis. Aβ2GPI antibodies induce higher platelet P-selectin expression during the active rather than the acute phases.