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@ARTICLE{Korn:127671,
      author       = {C. Korn$^*$ and B. Scholz$^*$ and J. Hu$^*$ and K.
                      Srivastava$^*$ and J. Wojtarowicz$^*$ and T. Arnsperger$^*$
                      and R. H. Adams and M. Boutros$^*$ and H. Augustin$^*$ and
                      I. Augustin$^*$},
      title        = {{E}ndothelial cell-derived non-canonical {W}nt ligands
                      control vascular pruning in angiogenesis.},
      journal      = {Development},
      volume       = {141},
      number       = {8},
      issn         = {1477-9129},
      address      = {Cambridge},
      publisher    = {The Company of Biologists},
      reportid     = {DKFZ-2017-03694},
      pages        = {1757 - 1766},
      year         = {2014},
      abstract     = {Multiple cell types involved in the regulation of
                      angiogenesis express Wnt ligands. Although β-catenin
                      dependent and independent Wnt signaling pathways have been
                      shown to control angiogenesis, the contribution of
                      individual cell types to activate these downstream pathways
                      in endothelial cells (ECs) during blood vessel formation is
                      still elusive. To investigate the role of ECs in
                      contributing Wnt ligands for regulation of blood vessel
                      formation, we conditionally deleted the Wnt secretion factor
                      Evi in mouse ECs (Evi-ECKO). Evi-ECKO mice showed decreased
                      microvessel density during physiological and pathological
                      angiogenesis in the postnatal retina and in tumors,
                      respectively. The reduced microvessel density resulted from
                      increased vessel regression accompanied by decreased EC
                      survival and proliferation. Concomitantly, survival-related
                      genes were downregulated and cell cycle arrest- and
                      apoptosis-inducing genes were upregulated. EVI silencing in
                      cultured HUVECs showed similar target gene regulation,
                      supporting a mechanism of EC-derived Wnt ligands in
                      controlling EC function. ECs preferentially expressed
                      non-canonical Wnt ligands and canonical target gene
                      expression was unaffected in Evi-ECKO mice. Furthermore, the
                      reduced vascularization of Matrigel plugs in Evi-ECKO mice
                      could be rescued by introduction of non-canonical Wnt5a.
                      Treatment of mouse pups with the non-canonical Wnt inhibitor
                      TNP470 resulted in increased vessel regression accompanied
                      by decreased EC proliferation, thus mimicking the
                      proliferation-dependent Evi-ECKO remodeling phenotype. Taken
                      together, this study identified EC-derived non-canonical Wnt
                      ligands as regulators of EC survival, proliferation and
                      subsequent vascular pruning during developmental and
                      pathological angiogenesis.},
      keywords     = {Cyclohexanes (NLM Chemicals) / DNA-Binding Proteins (NLM
                      Chemicals) / Evi1 protein, mouse (NLM Chemicals) / Ligands
                      (NLM Chemicals) / Sesquiterpenes (NLM Chemicals) /
                      Transcription Factors (NLM Chemicals) / Wnt Proteins (NLM
                      Chemicals) / O-(chloroacetylcarbamoyl)fumagillol (NLM
                      Chemicals)},
      cin          = {B110 / A190 / L101},
      ddc          = {570},
      cid          = {I:(DE-He78)B110-20160331 / I:(DE-He78)A190-20160331 /
                      I:(DE-He78)L101-20160331},
      pnm          = {322 - Genetics and Pathophysiology (POF3-322)},
      pid          = {G:(DE-HGF)POF3-322},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:24715464},
      doi          = {10.1242/dev.104422},
      url          = {https://inrepo02.dkfz.de/record/127671},
}