Abnormal blood vessel development and lethality in embryos lacking a single VEGF allele View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1996-04

AUTHORS

Peter Carmeliet, Valérie Ferreira, Georg Breier, Saskia Pollefeyt, Lena Kieckens, Marina Gertsenstein, Michaela Fahrig, Ann Vandenhoeck, Kendraprasad Harpal, Carmen Eberhardt, Cathérine Declercq, Judy Pawling, Lieve Moons, Désiré Collen, Werner Risau, Andras Nagy

ABSTRACT

THE endothelial cell-specific vascular endothelial growth factor (VEGF)1–5 and its cellular receptors Flt-1 (refs 6,7) and Flk-1 (refs 8,9) have been implicated in the formation of the embryonic vasculature. This is suggested by their colocalized expression during embryogenesis10,11 and the impaired vessel formation in Flk-1 (ref. 12) and Flt-1 (ref. 13) deficient embryos. However, because Flt-1 also binds placental growth factor14,15, a VEGF homologue, the precise role of VEGF was unknown. Here we report that formation of blood vessels was abnormal, but not abolished, in heterozygous VEGF-deficient (VEGF+/-) embryos, generated by aggregation of embryonic stem (ES) cells with tetraploid embryos (T-ES)16,17, and even more impaired in homozygous VEGF-deficient (VEGF-/-) T-ES embryos, resulting in death at mid-gestation. Similar phenotypes were observed in F1-VEGF-/- embryos, generated by germline transmission. We believe that this heterozygous lethal phenotype, which differs from the homozygous lethality in VEGF-receptor-deficient embryos, is unprecedented for a targeted autosomal gene inacti-vation, and is indicative of a tight dose-dependent regulation of embryonic vessel development by VEGF. More... »

PAGES

435-439

Journal

TITLE

Nature

ISSUE

6573

VOLUME

380

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/380435a0

    DOI

    http://dx.doi.org/10.1038/380435a0

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1034005847

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/8602241


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