A cell-based model of hemostasis

Based on our work and that of many other workers, we have developed a model of coagulation in vivo. Many workers have demonstrated mechanisms by which cells can influence the coagulation process. Nonetheless. the prevailing v iew of hemostasis remains that the protein coagulation factors direct and c ontrol the process with cells serving primarily to provide a phosphatidylse rine containing surface on which the procoagulant complexes are assembled. By contrast, we propose a model in which coagulation is regulated by proper ties of cell surfaces. This model emphasizes the importance of specific cel lular receptors for the coagulation proteins. Thus, cells with similar phos phatidylserine content can play very different roles in hemostasis dependin g on their complement of surface receptors. We propose that coagulation occ urs not as a "cascade", but in three overlapping stages: 1) initiation, whi ch occurs on a tissue factor bearing cell: 2) amplification, in which plate lets and cofactors an activated to set the stage for large scale thrombin g eneration: and 3) propagation, in which large amounts of thrombin are gener ated on the platelet surface. This cell based model explains some aspects o f hemostasis that a protein-centric model does not.