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Wound healing is a complex process initiated by the formationoffibrin fibers and endothelialization. Normally, this process is triggeredin a wound by thrombin cleavage of fibrinopeptides on fibrinogen molecules,which allows them to self spontaneously-assemble into large fibersthat provide the support structure of the clot and promote healing.We have found that the fibrous structures can also form without thrombinon most polymer or metal surfaces, including those commonly used forstents. We show that the relatively hydrophobic E and D regions ofthe fibrinogen molecule are adsorbed on these surfaces, exposing theαC domains, which in turn results in the formation of largefiber structures that promote endothelial cell adhesion. We show thatthe entire process can be suppressed when stents or other substratesare coated with polymers that are functionalized to bind the αCdomains, leading to the development of potentially nonthrombogenicimplant materials. [ABSTRACT FROM AUTHOR]