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@ARTICLE{Yang:127826,
      author       = {W.-J. Yang$^*$ and J. Hu$^*$ and A. Uemura and F.
                      Tetzlaff$^*$ and H. Augustin$^*$ and A. Fischer$^*$},
      title        = {{S}emaphorin-3{C} signals through {N}europilin-1 and
                      {P}lexin{D}1 receptors to inhibit pathological
                      angiogenesis.},
      journal      = {EMBO molecular medicine},
      volume       = {7},
      number       = {10},
      issn         = {1757-4684},
      address      = {Weinheim},
      publisher    = {Wiley-VCH},
      reportid     = {DKFZ-2017-03848},
      pages        = {1267 - 1284},
      year         = {2015},
      abstract     = {Retinopathy of prematurity causes visual impairment due to
                      destructive neoangiogenesis after degeneration of the
                      retinal microvasculature. This study was aimed at analyzing
                      whether local delivery of Semaphorin-3C (Sema3C) suppresses
                      pathological retinal angiogenesis. Sema3C exerted potent
                      inhibiting effects in cellular models of angiogenesis. In an
                      endothelial cell xenotransplantation assay, Sema3C acted
                      primarily on immature microvessels by inducing endothelial
                      cell apoptosis. Intravitreal administration of recombinant
                      Sema3C disrupted endothelial tip cell formation and
                      cell-cell contacts, which led to decreased vascular bed
                      expansion and vessel branching in the growing retinal
                      vasculature of newborn mice, while not affecting mature
                      vessels in the adult retina. Sema3C administration strongly
                      inhibited the formation of pathological pre-retinal vascular
                      tufts during oxygen-induced retinopathy. Mechanistically,
                      Sema3C signaled through the receptors Neuropilin-1 and
                      PlexinD1, which were strongly expressed on vascular tufts,
                      induced VE-cadherin internalization, and abrogated vascular
                      endothelial growth factor (VEGF)-induced activation of the
                      kinases AKT, FAK, and p38MAPK. This disrupted endothelial
                      cell junctions, focal adhesions, and cytoskeleton assembly
                      resulted in decreased cell migration and survival. Thus,
                      this study identified Sema3C as a potent and selective
                      inhibitor of pathological retinal angiogenesis.},
      keywords     = {Angiogenesis Inhibitors (NLM Chemicals) / Membrane
                      Glycoproteins (NLM Chemicals) / Nerve Tissue Proteins (NLM
                      Chemicals) / Plxnd1 protein, mouse (NLM Chemicals) /
                      Semaphorins (NLM Chemicals) / Neuropilin-1 (NLM Chemicals)},
      cin          = {A270 / A190},
      ddc          = {610},
      cid          = {I:(DE-He78)A270-20160331 / I:(DE-He78)A190-20160331},
      pnm          = {321 - Basic Concepts (POF3-321)},
      pid          = {G:(DE-HGF)POF3-321},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26194913},
      pmc          = {pmc:PMC4604683},
      doi          = {10.15252/emmm.201404922},
      url          = {https://inrepo02.dkfz.de/record/127826},
}