UCLA

Upstream exposure of platelets to activating proteins primes platelets for increased downstream adhesion, though the mechanics of platelet translocation before permanently arresting are not well understood. To investigate platelet translocation on platelet-binding proteins, primed platelets transient contacts with immobilized proteins were recorded and analyzed. Using a microfluidic channel, representative of a vascular graft, platelet-activating proteins were covalently attached to the upstream priming, center, and downstream capture positions. Image sequences of platelet interactions with the center protein were captured as platelet-rich plasma (PRP) was perfused through the channel. There was an increase in both platelet pause events and net platelet adhesion on von Willebrand factor, collagen, or fibrinogen following upstream exposure to the same protein. Upstream priming also caused a decrease in average platelet velocity. The duration of transient platelet arrests on the protein-coated surface and the distance that platelets travel between pause events depended on the protein with which they were interacting. The most significant increase in platelet pause events frequency and decrease in average velocity occurred on immobilized von Willebrand factor, compared to the control with no upstream priming. These results demonstrate that platelet priming increases downstream platelet-protein interactions prior to permanent adhesion.