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Prepublished online as a Blood First Edition Paper on October 24, 2002; DOI 10.1182/blood-2002-01-0119. This Article Full Text (PDF) All Versions of this Article: 2002-01-0119v1 101/5/1801    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Yamada, Y. Articles by Takakura, N. Search for Related Content PubMed PubMed Citation Articles by Yamada, Y. Articles by Takakura, N. Social Bookmarking                   What's this? Submitted January 16, 2002 Accepted October 17, 2002 Neuropilin-1 on hematopoietic cells as a source of vascular development Yoshihiro Yamada, Yuichi Oike, Hisao Ogawa, Yasuhiro Ito, Hajime Fijisawa, Toshio Suda, and Nobuyuki Takakura* The Sakaguchi Laboratory of Developmental Biology, Keio University School of Medicine, Tokyo, Japan; Department of Cell Differentiation, Kumamoto University School of Medicine, Institute of Molecular Embryology and Genetics, Kumamoto, Japan; Department of Cardiovascular Medicine, Kumamoto University School of Medicine, Kumamoto, Japan Division of Biological Science, Group of Developmental Neurobiology, Nagoya University Graduate School of Science, Nagoya, Japan; Department of Stem Cell Biology, Kanazawa University Cancer Research Institute, Kanazawa, Japan * Corresponding author; email: ntakaku{at}kenroku.kanazawa-u.ac.jp. Neuropilin-1 (NP-1) is a receptor for vascular endothelial growth factor-165 (VEGF165) and acts as a coreceptor that enhances the function of VEGF165 through VEGFR-2. Studies using transgenic and knockout mice of NP-1 indicated that this molecule is important for vascular development as well as neuronal development. We recently reported that clustered soluble NP-1 phosphorylates VEGFR-2 on endothelial cells with a low dose of VEGF165, and rescues the defective vascularity of the NP-1-/- embryo in vitro and in vivo. Here we show that NP-1 is expressed by CD45+ hematopoietic cells in the fetal liver, can bind VEGF165, and phosphorylates VEGFR-2 on endothelial cells. CD45+NP-1+ cells rescued the defective vasculogenesis and angiogenesis in the NP-1-/- P-Sp culture, although CD45+NP-1- cells did not. Moreover, CD45+NP-1+ cells together with VEGF165 induced angiogenesis in an in vivo matrigel assay and cornea neovascularization assay. The extracellular domain of NP-1 consists of "a", "b" and "c" domains and it is known that the "a" and "c" domains are necessary for dimerization of NP-1. We found that both the "a" and "c" domains are essential for such rescue of defective vascularities in the NP-1 mutant. These results suggest that NP-1 enhances vascular development exogenously and that dimerization of NP-1 is important for such effect. In NP-1-/- embryos, vascular sprouting is impaired at the CNS and pericardium where VEGF is not abundant, indicating that NP-1-expressing cells are required for normal vascular development. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D.-H. Yang, J.-Y. Yoon, S.-H. Lee, V. Bryja, E. R. Andersson, E. Arenas, Y.-G. Kwon, and K.-Y. 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