Key result
Endothelial PAR1 expression rescues Par1-/- embryos, preventing ~50% midgestational bleeding-related lethality.
The coagulation protease thrombin triggers fibrin formation, platelet activation, and other cellular responses at sites of tissue injury. We report a role for PAR1, a protease-activated G protein-coupled receptor for thrombin, in embryonic development. Approximately half of Par1-/- mouse embryos died at midgestation with bleeding from multiple sites. PAR1 is expressed in endothelial cells, and a PAR1 transgene driven by an endothelial-specific promoter prevented death of Par1-/- embryos. Our results suggest that the coagulation cascade and PAR1 modulate endothelial cell function in developing blood vessels and that thrombin's actions on endothelial cells-rather than on platelets, mesenchymal cells, or fibrinogen-contribute to vascular development and hemostasis in the mouse embryo.
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Griffin et al. (2001) studied Embryonic death and bleeding. PAR1 transgene driven by an endothelial-specific promoter vs. Par1-/- without transgene was evaluated on Death at midgestation with bleeding. An endothelial-specific PAR1 transgene prevented death in Par1-/- mouse embryos, where approximately half otherwise died at midgestation with bleeding from multiple sites.
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