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Exposure of membrane phosphatidylserine and platelet procoagulant activity Volume 13, issue 2, Mars-Avril 2007

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INSERM U770, Hôpital de Bicêtre, Université Paris Sud, Faculté de médecine, 80 rue du Général Leclerc, 94276 Le Kremlin-Bicêtre Cedex

Platelet acquisition of procoagulant phenotype is central to haemostasis, and is associated with redistribution of phospholipids between the two leaflets of plasma membranes. Upon procoagulant activation, cell surface exposure of phosphatidylserine (PS) – an anionic phospholipid normally sequestered in the cytoplasmic leaflet of resting cells – favours assembly of the coagulation enzyme complexes. The essential role of PS surface exposure in haemostasis is illustrated by the Scott syndrome, a rare bleeding disorder characterized by defective PS rapid redistribution in haematopoietic cells. Considering that exceeding platelet procoagulant activity is, conversely, associated with increased risk for thrombosis, the identification of effectors of procoagulant membrane plasticity as well as the characterization of the molecular defect(s) associated with Scott syndrome are important goals in haematology research and drug design. This review aims at presenting the current knowledge on the molecular effectors of membrane procoagulant remodelling associated with PS cell surface exposure. Attempt is made to specify among the various mechanisms those effective in normal haematopoietic cells and defective in cells from Scott syndrome patients.