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. 1997 Nov;151(5):1199–1204.

Mice lacking the thrombin receptor, PAR1, have normal skin wound healing.

A J Connolly 1, D Y Suh 1, T K Hunt 1, S R Coughlin 1
PMCID: PMC1858088  PMID: 9358744

Abstract

Thrombin's actions on platelets, macrophages, fibroblasts, and endothelial cells have prompted the hypothesis that thrombin may be important for inflammatory and fibroproliferative processes in wound healing. Protease-activated receptor 1 (PAR1) is a G-protein-coupled receptor that mediates many of the cellular activities of thrombin. To test the role of this receptor in vivo, we generated PAR1-deficient mice. Despite the observation that fibroblasts cultured from these mice lacked responsiveness to thrombin in vitro, we now report that there was no difference detected between wild-type and PAR1-deficient mice in skin wound healing assays including time to closure of open wounds, tensile strength 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.

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Selected References

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