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@ARTICLE{Leibing:136954,
      author       = {T. Leibing and C. Géraud and I. Augustin$^*$ and M.
                      Boutros$^*$ and H. Augustin$^*$ and J. G. Okun and C.-D.
                      Langhans and J. Zierow and S. A. Wohlfeil and V. Olsavszky
                      and K. Schledzewski and S. Goerdt and P.-S. Koch},
      title        = {{A}ngiocrine {W}nt signaling controls liver growth and
                      metabolic maturation in mice.},
      journal      = {Hepatology},
      volume       = {68},
      number       = {2},
      issn         = {0270-9139},
      address      = {New York [u.a.]},
      publisher    = {Wiley Interscience},
      reportid     = {DKFZ-2018-01383},
      pages        = {707 - 722},
      year         = {2018},
      note         = {DKFZ-ZMBH Alliance},
      abstract     = {Postnatal liver development is characterized by hepatocyte
                      growth, proliferation, and functional maturation. Notably,
                      canonical Wnt signaling in hepatocytes has been identified
                      as an important regulator of final adult liver size and
                      metabolic liver zonation. The cellular origin of Wnt ligands
                      responsible for homeostatic liver/body weight ratio (LW/BW)
                      remained unclear, which was also attributable to a lack of
                      suitable endothelial Cre driver mice. To comprehensively
                      analyze the effects of hepatic angiocrine Wnt signaling on
                      liver development and metabolic functions, we used
                      endothelial subtype-specific Stab2-Cre driver mice to delete
                      Wls from hepatic endothelial cells (HECs). The resultant
                      Stab2-Cretg/wt ;Wlsfl/fl (Wls-HECKO) mice were viable, but
                      showed a significantly reduced LW/BW. Specifically, ablation
                      of angiocrine Wnt signaling impaired metabolic zonation in
                      the liver, as shown by loss of pericentral,
                      β-catenin-dependent target genes such as glutamine synthase
                      (Glul), RhBg, Axin2, and cytochrome P450 2E1, as well as by
                      extended expression of periportal genes such as arginase 1.
                      Furthermore, endothelial subtype-specific expression of a
                      c-terminally YFP-tagged Wls fusion protein in Wls-HECKO mice
                      (Stab2-Cretg/wt ;Wlsfl/fl ;Rosa26:Wls-YFPfl/wt [Wls-rescue])
                      restored metabolic liver zonation. Interestingly, lipid
                      metabolism was altered in Wls-HECKO mice exhibiting
                      significantly reduced plasma cholesterol levels, while
                      maintaining normal plasma triglyceride and blood glucose
                      concentrations. On the contrary, zonal expression of
                      Endomucin, LYVE1, and other markers of HEC heterogeneity
                      were not altered in Wls-HECKO livers.Angiocrine Wnt
                      signaling controls liver growth as well as development of
                      metabolic liver zonation in mice, whereas intrahepatic HEC
                      zonation is not affected. (Hepatology 2017).},
      cin          = {B110 / A190},
      ddc          = {610},
      cid          = {I:(DE-He78)B110-20160331 / I:(DE-He78)A190-20160331},
      pnm          = {321 - Basic Concepts (POF3-321)},
      pid          = {G:(DE-HGF)POF3-321},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29059455},
      pmc          = {pmc:PMC6099291},
      doi          = {10.1002/hep.29613},
      url          = {https://inrepo02.dkfz.de/record/136954},
}