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The podoplanin-CLEC-2 axis is critical in mice for prevention of hemorrhage in the cerebral vasculature during mid-gestation. This raises the question as to how platelets are captured by podoplanin on neuroepithelial cells in a high shear environment. In this study, we demonstrate that mouse platelets form stable aggregates on mouse podoplanin at arterial shear through a CLEC-2 and Src kinase-dependent pathway. Adhesion and aggregation are also dependent on the platelet glycoprotein (GP) receptors, integrin αIIbβ3 and GPIb, and the feedback agonists ADP and thromboxane A2 (TxA2). CLEC-2 does not bind to von Willebrand factor (VWF) suggesting that the interaction with podoplanin is sufficient to both tether and activate platelets. Consistent with this, the surface plasmon resonance measurements reveal that mouse CLEC-2 binds to mouse podoplanin with nanomolar affinity. The present findings demonstrate a novel pathway of hemostasis in which podoplanin supports platelet capture and activation at arteriolar rates of shear.

Original publication




Journal article



Publication Date





716 - 722


CLEC-2, Capillary flow assay, platelet activation, platelet aggregation, podoplanin, Animals, Biomarkers, Biomechanical Phenomena, Blood Platelets, Endothelial Cells, Gene Expression, Hemostasis, Humans, Lectins, C-Type, Membrane Glycoproteins, Mice, Platelet Activation, Platelet Adhesiveness, Platelet Aggregation, Protein Binding, Recombinant Fusion Proteins