Mice lacking factor VII develop normally but suffer fatal perinatal bleeding

Elliot D. Rosen, Joyce C. Y. Chan, Esohe Idusogie, Frédéric Clotman, George Vlasuk, Thomas Luther, Louise R. Jalbert, Sybille Albrecht, Liang Zhong, Ann Lissens, Luc Schoonjans, Lieve Moons, Désiré Collen (), Francis J. Castellino and Peter Carmeliet
Additional contact information
Elliot D. Rosen: Center for Transgene Technology and Gene Therapy, Flanders Interuniversity Institute for Biotechnology
Joyce C. Y. Chan: Center for Transgene Technology and Gene Therapy, Flanders Interuniversity Institute for Biotechnology
Esohe Idusogie: Center for Transgene Technology and Gene Therapy, Flanders Interuniversity Institute for Biotechnology
Frédéric Clotman: Laboratory of Developmental Genetics, University of Louvain
George Vlasuk: Corvas International Inc., San Diego
Thomas Luther: Institute of Pathology, Technical University of Dresden
Louise R. Jalbert: Center for Transgene Technology and Gene Therapy, Flanders Interuniversity Institute for Biotechnology
Sybille Albrecht: Institute of Pathology, Technical University of Dresden
Liang Zhong: Center for Transgene Technology and Gene Therapy, Flanders Interuniversity Institute for Biotechnology
Ann Lissens: Center for Transgene Technology and Gene Therapy, Flanders Interuniversity Institute for Biotechnology
Luc Schoonjans: Center for Transgene Technology and Gene Therapy, Flanders Interuniversity Institute for Biotechnology
Lieve Moons: Center for Transgene Technology and Gene Therapy, Flanders Interuniversity Institute for Biotechnology
Désiré Collen: Center for Transgene Technology and Gene Therapy, Flanders Interuniversity Institute for Biotechnology
Francis J. Castellino: Center for Transgene Research, University of Notre Dame
Peter Carmeliet: Center for Transgene Technology and Gene Therapy, Flanders Interuniversity Institute for Biotechnology

Nature, 1997, vol. 390, issue 6657, 290-294

Abstract: Abstract Blood coagulation in vivo is initiated by factor VII (FVII) binding to its cellular receptor tissue factor (TF)1,2,3,4. FVII is the only known ligand for TF, so it was expected that FVII-deficient embryos would have a similar phenotype to TF-deficient embryos, which have defective vitello-embryonic circulation and die around 9.5 days of gestation5,6,7,8. Surprisingly, we find that FVII-deficient (FVII−/−) embryos developed normally. FVII−/− mice succumbed perinatally because of fatal haemorrhaging from normal blood vessels. At embryonic day 9.5, maternal–fetal transfer of FVII was undetectable and survival of embryos did not depend on TF–FVII-initiated fibrin formation. Thus, the TF−/− embryonic lethal and the FVII−/− survival-phenotypes suggest a role for TF during embryogenesis beyond fibrin formation.

Date: 1997
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DOI: 10.1038/36862

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