Abstract
Mice deficient in the Flk-1 receptor tyrosine kinase are known to die in utero because of defective vascular and hematopoietic development. Here, we show that flk-1(-/-) embryonic stem cells are nevertheless able to differentiate into hematopoietic and endothelial cells in vitro, although they give rise to a greatly reduced number of blast colonies, a measure of hemangioblast potential. Furthermore, normal numbers of hematopoietic progenitors are found in 7.5-day postcoitum flk-1(-/-) embryos, even though 8. 5-day postcoitum flk-1(-/-) embryos are known to be deficient in such cells. Our results suggest that hematopoietic/endothelial progenitors arise independently of Flk-1, but that their subsequent migration and expansion require a Flk-1-mediated signal.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Cell Adhesion
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Cells, Cultured
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Embryo, Mammalian
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Endothelium, Vascular / cytology
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Endothelium, Vascular / physiology*
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Flow Cytometry
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Gene Expression Regulation, Developmental*
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Hematopoietic Stem Cells / cytology
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Hematopoietic Stem Cells / physiology*
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Mice
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Mice, Knockout
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Receptor Protein-Tyrosine Kinases / deficiency
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Receptor Protein-Tyrosine Kinases / genetics
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Receptor Protein-Tyrosine Kinases / physiology*
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Receptors, Growth Factor / deficiency
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Receptors, Growth Factor / genetics
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Receptors, Growth Factor / physiology*
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Receptors, Mitogen / physiology
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Receptors, Vascular Endothelial Growth Factor
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Reverse Transcriptase Polymerase Chain Reaction
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Signal Transduction
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Stem Cells / physiology*
Substances
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Receptors, Growth Factor
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Receptors, Mitogen
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Receptor Protein-Tyrosine Kinases
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Receptors, Vascular Endothelial Growth Factor