VWF (von Willebrand Factor) Comes in From the Cold As a Strategy to Improve Platelet Storage.

Abstract

The interaction between platelet GPIb (glycoprotein Ib) and VWF (von Willebrand factor) is essential for blood hemostasis and occurs when VWF is bound to damaged subendothelium representing the first step in platelet adhesion. The interaction is mediated between the N-terminal domain of GPIb and the VWF A1 domain and does not normally occur under static conditions requiring high hydrodynamic shear stress to stimulate the binding by unfolding VWF. In clinical settings where the hemostatic system needs a boost such as hemorrhage or low platelet counts (thrombocytopenia) transfusion of platelets is a desirable therapeutic option. However, storing platelets for transfusion at room temperature presents a problem as there is an increased risk of microbial infection. Thus, refrigerated platelet storage is a superior alternative, but cold treatment leads to rapid platelet clearance after transfusion. Recent studies from the group of Renhao Li using a variety of approaches confirmed the findings from previous work1,2 showing the importance of the GPIb receptor as a driver of cold platelet clearance.3 In addition, they implicated the interaction with ligand (VWF) as making a significant contribution to the clearance mechanism.3 The same group then reported that the OS1 (optimized sequence 1) peptide, which binds to GPIb, and is a highly selective and potent inhibitor of the interaction with VWF when added during platelet refrigeration improved the recovery and survival of platelets.4