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@ARTICLE{Graud:120363,
      author       = {C. Géraud and P.-S. Koch and J. Zierow and K.
                      Klapproth$^*$ and K. Busch$^*$ and V. Olsavszky and T.
                      Leibing and A. Demory and F. Ulbrich and M. Diett and S.
                      Singh and C. Sticht and K. Breitkopf-Heinlein and K.
                      Richter$^*$ and S.-M. Karppinen and T. Pihlajaniemi and B.
                      Arnold$^*$ and H.-R. Rodewald$^*$ and H. Augustin$^*$ and K.
                      Schledzewski and S. Goerdt},
      title        = {{GATA}4-dependent organ-specific endothelial
                      differentiation controls liver development and embryonic
                      hematopoiesis.},
      journal      = {The journal of clinical investigation},
      volume       = {127},
      number       = {3},
      issn         = {1558-8238},
      address      = {Ann Arbor, Mich.},
      publisher    = {ASCJ},
      reportid     = {DKFZ-2017-00797},
      pages        = {1099 - 1114},
      year         = {2017},
      abstract     = {Microvascular endothelial cells (ECs) are increasingly
                      recognized as organ-specific gatekeepers of their
                      microenvironment. Microvascular ECs instruct neighboring
                      cells in their organ-specific vascular niches through
                      angiocrine factors, which include secreted growth factors
                      (angiokines), extracellular matrix molecules, and
                      transmembrane proteins. However, the molecular regulators
                      that drive organ-specific microvascular transcriptional
                      programs and thereby regulate angiodiversity are largely
                      elusive. In contrast to other ECs, which form a continuous
                      cell layer, liver sinusoidal ECs (LSECs) constitute
                      discontinuous, permeable microvessels. Here, we have shown
                      that the transcription factor GATA4 controls murine LSEC
                      specification and function. LSEC-restricted deletion of
                      Gata4 caused transformation of discontinuous liver sinusoids
                      into continuous capillaries. Capillarization was
                      characterized by ectopic basement membrane deposition,
                      formation of a continuous EC layer, and increased expression
                      of VE-cadherin. Correspondingly, ectopic expression of GATA4
                      in cultured continuous ECs mediated the downregulation of
                      continuous EC-associated transcripts and upregulation of
                      LSEC-associated genes. The switch from discontinuous LSECs
                      to continuous ECs during embryogenesis caused liver
                      hypoplasia, fibrosis, and impaired colonization by
                      hematopoietic progenitor cells, resulting in anemia and
                      embryonic lethality. Thus, GATA4 acts as master regulator of
                      hepatic microvascular specification and acquisition of
                      organ-specific vascular competence, which are indispensable
                      for liver development. The data also establish an essential
                      role of the hepatic microvasculature in embryonic
                      hematopoiesis.},
      cin          = {D110 / A190 / W230 / D050},
      ddc          = {610},
      cid          = {I:(DE-He78)D110-20160331 / I:(DE-He78)A190-20160331 /
                      I:(DE-He78)W230-20160331 / I:(DE-He78)D050-20160331},
      pnm          = {321 - Basic Concepts (POF3-321)},
      pid          = {G:(DE-HGF)POF3-321},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28218627},
      pmc          = {pmc:PMC5330741},
      doi          = {10.1172/JCI90086},
      url          = {https://inrepo02.dkfz.de/record/120363},
}