Rational design of ex vivo model of thrombosis Public Deposited

http://ir.library.oregonstate.edu/concern/undergraduate_thesis_or_projects/3x816p399

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  • When vessel walls within the vasculature are damaged, exposed extracellular matrix (ECM) proteins trigger a series of events that lead to the formation of a hemostatic plug (Andrews et al. 2004, Furie et al. 2008, Watson 2009). Thrombus formation requires an orchestrated series of receptor-mediated events facilitating platelet recruitment, platelet activation, and initiation of coagulation. This process ultimately leads to thrombin generation and thrombus formation. In diseased vessels, this process leads to the propagation of intravascular thrombus formation and vessel occlusion, which is the underlying cause of cardiovascular disease. We have developed a model of occlusive thrombus formation that relies on gravity to drive blood flow through a capillary tube under a constant pressure gradient. We have used this model to identify a role for laminin in the formation of occlusive thrombi in a FXII-dependent manner. We have also used this model to characterize the procoagulant phenotype of breast cancer epithelial cell lines in the presence of physiologically relevant, pressure-driven blood flow. The use of this model may be expanded to characterize the mechanisms of thrombosis and to determine the efficacy of pharmacological agents designed to prevent occlusive thrombus formation.
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