MICE LACKING THE THROMBIN RECEPTOR, PAR1, HAVE NORMAL SKIN WOUND-HEALING

Thrombin's actions on platelets, macrophages, fibroblasts, and endothe lial cells have prompted the hypothesis that thrombin may be important for inflammatory and fibroproliferative processes in wound healing. P rotease-activated receptor 1 (PAR1) is a G-protein-coupled receptor th at mediates many of the cellular activities of thrombin. To test the r ole of this receptor in vivo, we generated PAR1-deficient mice. Despit e the observation that fibroblasts cultured from these mice lacked res ponsiveness to thrombin in vitro, we now report that there was no diff erence detected between wild-type and PAR1-deficient mice in skin woun d healing assays including time to closure of open wounds, tensile str ength of healed incisional wounds, wound histology, and hydroxyproline /DNA content of wound implants. We conclude that PAR1 is not necessary for normal skin wound healing in mice.