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Publication Detail
Vascular endothelial growth factor receptor 3 directly regulates murine neurogenesis.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Calvo C-F, Fontaine RH, Soueid J, Tammela T, Makinen T, Alfaro-Cervello C, Bonnaud F, Miguez A, Benhaim L, Xu Y, Barallobre M-J, Moutkine I, Lyytikkä J, Tatlisumak T, Pytowski B, Zalc B, Richardson W, Kessaris N, Garcia-Verdugo JM, Alitalo K, Eichmann A, Thomas J-L
  • Publication date:
    15/04/2011
  • Pagination:
    831, 844
  • Journal:
    Genes Dev
  • Volume:
    25
  • Issue:
    8
  • Status:
    Published
  • Country:
    United States
  • PII:
    25/8/831
  • Language:
    eng
  • Keywords:
    Animals, Cells, Cultured, Enzyme-Linked Immunosorbent Assay, Immunohistochemistry, Lymphangiogenesis, Mice, Mice, Mutant Strains, Microscopy, Electron, Transmission, Neovascularization, Physiologic, Neural Stem Cells, Neurogenesis, Oligonucleotide Array Sequence Analysis, Reverse Transcriptase Polymerase Chain Reaction, Vascular Endothelial Growth Factor Receptor-3
Abstract
Neural stem cells (NSCs) are slowly dividing astrocytes that are intimately associated with capillary endothelial cells in the subventricular zone (SVZ) of the brain. Functionally, members of the vascular endothelial growth factor (VEGF) family can stimulate neurogenesis as well as angiogenesis, but it has been unclear whether they act directly via VEGF receptors (VEGFRs) expressed by neural cells, or indirectly via the release of growth factors from angiogenic capillaries. Here, we show that VEGFR-3, a receptor required for lymphangiogenesis, is expressed by NSCs and is directly required for neurogenesis. Vegfr3:YFP reporter mice show VEGFR-3 expression in multipotent NSCs, which are capable of self-renewal and are activated by the VEGFR-3 ligand VEGF-C in vitro. Overexpression of VEGF-C stimulates VEGFR-3-expressing NSCs and neurogenesis in the SVZ without affecting angiogenesis. Conversely, conditional deletion of Vegfr3 in neural cells, inducible deletion in subventricular astrocytes, and blocking of VEGFR-3 signaling with antibodies reduce SVZ neurogenesis. Therefore, VEGF-C/VEGFR-3 signaling acts directly on NSCs and regulates adult neurogenesis, opening potential approaches for treatment of neurodegenerative diseases.
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Wolfson Inst for Biomedical Research
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