THE ROLE OF THROMBIN, FIBRINOGEN, AND FIBRONECTIN ON PLATELET CLOT RETRACTION FORCES ANALYZED USING MICROPOSTS

摘要

When a blood vessel is damaged, platelets aggregate together to form a thrombus that seals vascular leakage and promotes healing. The process of thrombosis involves activation of platelets by soluble ligands, adhesion to the wound site, change in shape from a discoidal to a stellate structure, and the attachment of additional platelets onto the nascent clot through adhesive ligand bridges. Once formed, a clot will undergo a retraction in volume that packs platelets together and allows blood flow to recommence. Much attention has been paid to the early phases of thrombosis - adhesion and aggregation - but the process of clot retraction is vital to stabilizing the clot. We have developed a new microscale approach using microposts to measure platelet retraction forces that allows for new insight into the biomechanics of clot formation. Platelets generate contractile forces through actin-myosin interactions that lead to clot retraction and stability [1]. If platelets are unable to generate forces, then the clots they form are loosely-bound and may detach and cause an embolism. Likewise, a higher propensity toward contractility by platelets may cause excessive clot formation in arteries and block blood flow.