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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 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 Citation Map 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. Related Collections Hematopoiesis and Stem Cells Hemostasis, Thrombosis, and Vascular Biology Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 March 2003, Vol. 101, No. 5, pp. 1801-1809 HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Neuropilin-1 on hematopoietic cells as a source of vascular development Yoshihiro Yamada, Yuichi Oike, Hisao Ogawa, Yasuhiro Ito, Hajime Fujisawa, Toshio Suda, and Nobuyuki Takakura From the Sakaguchi Laboratory of Developmental Biology, Keio University School of Medicine, Tokyo; Department of Cell Differentiation, Institute of Molecular Embryology and Genetics and Department of Cardiovascular Medicine, Kumamoto University School of Medicine; Group of Developmental Neurobiology, Division of Biological Science, Nagoya University Graduate School of Science; and Department of Stem Cell Biology, Cancer Research Institute, Kanazawa University, Japan. 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 VEGF receptor-2 (VEGFR-2). Studies using transgenic and knock-out 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 (para-aortic splanchnopleural mesodermal region) 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 vasculogenesis and angiogenesis exogenously and that dimerization of NP-1 is important for enhancing vascular development. In NP-1/ embryos, vascular sprouting is impaired at the central nervous system (CNS) and pericardium where VEGF is not abundant, indicating that NP-1-expressing cells are required for normal vascular development. © 2003 by The American Society of Hematology.   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. 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