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Correspondence to: José A. López, Veterans Affairs Medical Center, Hematology/Oncology (111H), 2002 Holcombe Blvd., Houston, TX 77030. Tel:713-794-7088 Fax:713-794-7578 E-mail:josel{at}bcm.tmc.edu.
We have identified platelet glycoprotein (GP) Ib
as a counterreceptor for P-selectin. GP Ib
is a component of the GP Ib-IX-V complex, which mediates platelet adhesion to subendothelium at sites of injury. Cells expressing P-selectin adhered to immobilized GP Ib
, and GP Ib
–expressing cells adhered to and rolled on P-selectin and on histamine-stimulated endothelium in a P-selectindependent manner. In like manner, platelets rolled on activated endothelium, a phenomenon inhibited by antibodies to both P-selectin and GP Ib
. Unlike the P-selectin interaction with its leukocyte ligand, PSGL-1 (P-selectin glycoprotein ligand 1), the interaction with GP Ib
required neither calcium nor carbohydrate core-2 branching or
(1,3)-fucosylation. The interaction was inhibited by sulfated proteoglycans and by antibodies against GP Ib
, including one directed at a tyrosine-sulfated region of the polypeptide. Thus, the GP Ib-IX-V complex mediates platelet attachment to both subendothelium and activated endothelium.
Key Words: platelet adhesion, endothelium, platelet glycoproteins, selectins, PSGL-1
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