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Keratin hydrogel increases survival time in femoral artery injury model via potential platelet adhesion mechanism
Author(s) -
Rouse Jillian,
Burnett Luke,
Orebaugh Clinton,
Stahle Mary,
Hantgan Roy,
Van Dyke Mark
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.638.4
Subject(s) - hemostasis , self healing hydrogels , platelet , keratin , adhesion , chemistry , wound healing , platelet activation , platelet adhesiveness , microbiology and biotechnology , immunology , medicine , pathology , surgery , biology , platelet aggregation , polymer chemistry , organic chemistry
Keratin hydrogel is shown to be hemostatic in a porcine lethal extremity hemorrhage model compared to gauze and HemCon control groups with the presumptive mechanism of action being platelet adhesion and aggregation. Results showed that keratin hydrogels reduced shock index and increased survival time in comparison to both HemCon and gauze. Experiments to elucidate the mechanism of keratin hemostasis showed that platelets readily adhered to hydrogel films and that adherent cells contained numerous pseudopods, indicative of activation. Studies employing integrin function‐blocking antibodies reduced platelet adhesion. Collectively, these studies indicate that keratin promotes hemostasis via platelet adhesion by an integrin‐mediated process. Keratin hydrogels were shown to promote hemostasis and increase survival time in a lethal hemorrhage model with platelet adhesion and activation as the likely basis for the hemostatic property of keratin biomaterials. This work was supported by the US Army, SNS Nanofiber Technologies, American Heart Association, and Mid‐Atlantic Affiliate Grant‐in‐Aid.