| First Author | Connolly AJ | Year | 1997 |
| Journal | Am J Pathol | Volume | 151 |
| Issue | 5 | Pages | 1199-204 |
| PubMed ID | 9358744 | Mgi Jnum | J:43850 |
| Mgi Id | MGI:1099039 | Citation | Connolly AJ, et al. (1997) Mice lacking the thrombin receptor, PAR1, have normal skin wound healing. Am J Pathol 151(5):1199-204 |
| abstractText | 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. |
