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

Submitted: 21 November 2011
Accepted: 30 November 2011
Published: 19 March 2012
Abstract Views: 1323
PDF: 623
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Authors

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.

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Citations

A. Bontadi, Cattedra e UOC di Reumatologia
Dipartimento di Medicina Clinica e Sperimentale

How to Cite

Bontadi, A., Ruffatti, A., Giannini, S., Falcinelli, E., Tonello, M., Hoxha, A., … Punzi, L. (2012). In vitro effect of anti-β2 glycoprotein I antibodies on P-selectin expression, a marker of platelet activation. Reumatismo, 64(1), 35–39. https://doi.org/10.4081/reumatismo.2012.35

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