Inhibiting GPIbα Shedding Preserves Post-Transfusion Recovery and Hemostatic Function of Platelets After Prolonged Storage
Author(s) -
Wenchun Chen,
Xin Liang,
Anum Syed,
Paula Jessup,
William R. Church,
Jerry Ware,
Cassandra D. Josephson,
Renhao Li
Publication year - 2016
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.116.307639
Subject(s) - platelet , platelet glycoprotein gpib ix complex , platelet transfusion , platelet activation , chemistry , ex vivo , in vivo , platelet membrane glycoprotein , immunology , thrombus , von willebrand factor , medicine , biology , biochemistry , in vitro , microbiology and biotechnology
The platelet storage lesion accelerates platelet clearance after transfusion, but the underlying molecular mechanism remains elusive. Although inhibiting sheddase activity hampers clearance of platelets with storage lesion, the target platelet protein responsible for ectodomain shedding-induced clearance is not definitively identified. Monoclonal antibody 5G6 was developed recently to bind specifically human platelet receptor glycoprotein (GP)Ibα and inhibit its shedding but not shedding of other receptors. Here, the role of GPIbα shedding in platelet clearance after transfusion was addressed.
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