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@ARTICLE{Mogler:127165,
      author       = {C. Mogler$^*$ and M. Wieland$^*$ and C. König$^*$ and J.
                      Hu and A. Runge$^*$ and C. Korn$^*$ and E. Besemfelder$^*$
                      and K. Breitkopf-Heinlein and D. Komljenovic$^*$ and S.
                      Dooley and P. Schirmacher and T. Longerich and H.
                      Augustin$^*$},
      title        = {{H}epatic stellate cell-expressed endosialin balances
                      fibrogenesis and hepatocyte proliferation during liver
                      damage.},
      journal      = {EMBO molecular medicine},
      volume       = {7},
      number       = {3},
      issn         = {1757-4684},
      address      = {Weinheim},
      publisher    = {Wiley-VCH},
      reportid     = {DKFZ-2017-03191},
      pages        = {332 - 338},
      year         = {2015},
      abstract     = {Liver fibrosis is a reversible wound-healing response to
                      injury reflecting the critical balance between liver repair
                      and scar formation. Chronic damage leads to progressive
                      substitution of liver parenchyma by scar tissue and
                      ultimately results in liver cirrhosis. Stromal cells
                      (hepatic stellate cells [HSC] and endothelial cells) have
                      been proposed to control the balance between liver fibrosis
                      and regeneration. Here, we show that endosialin, a C-type
                      lectin, expressed in the liver exclusively by HSC and portal
                      fibroblasts, is upregulated in liver fibrosis in mouse and
                      man. Chronic chemically induced liver damage resulted in
                      reduced fibrosis and enhanced hepatocyte proliferation in
                      endosialin-deficient (EN(KO)) mice. Correspondingly,
                      acute-liver-damage-induced hepatocyte proliferation (partial
                      hepatectomy) was increased in EN(KO) mice. A candidate-based
                      screen of known regulators of hepatocyte proliferation
                      identified insulin-like growth factor 2 (IGF2) as
                      selectively endosialin-dependent hepatocyte mitogen.
                      Collectively, the study establishes a critical role of HSC
                      in the reciprocal regulation of fibrogenesis vs. hepatocyte
                      proliferation and identifies endosialin as a therapeutic
                      target in non-neoplastic settings.},
      keywords     = {Antigens, CD (NLM Chemicals) / Antigens, Neoplasm (NLM
                      Chemicals) / CD248 protein, human (NLM Chemicals) / Neoplasm
                      Proteins (NLM Chemicals) / tumor endothelial marker 1, mouse
                      (NLM Chemicals)},
      cin          = {A190 / L101 / E020},
      ddc          = {610},
      cid          = {I:(DE-He78)A190-20160331 / I:(DE-He78)L101-20160331 /
                      I:(DE-He78)E020-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25680861},
      pmc          = {pmc:PMC4364949},
      doi          = {10.15252/emmm.201404246},
      url          = {https://inrepo02.dkfz.de/record/127165},
}