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@ARTICLE{BreitkopfHeinlein:120514,
      author       = {K. Breitkopf-Heinlein and C. Meyer and C. König$^*$ and H.
                      Gaitantzi and A. Addante and M. Thomas and E. Wiercinska and
                      C. Cai and Q. Li and F. Wan and C. Hellerbrand and N.
                      Valous$^*$ and M. Hahnel and C. Ehlting and J. G. Bode and
                      S. Müller-Bohl$^*$ and U. Klingmüller$^*$ and J.
                      Altenöder and I. Ilkavets and M.-J. Goumans and L. J. A. C.
                      Hawinkels and S.-J. Lee and M. Wieland$^*$ and C. Mogler and
                      M. P. Ebert and B. Herrera and H. Augustin$^*$ and A.
                      Sánchez and S. Dooley and P. Ten Dijke},
      title        = {{BMP}-9 interferes with liver regeneration and promotes
                      liver fibrosis.},
      journal      = {Gut},
      volume       = {66},
      number       = {5},
      issn         = {1468-3288},
      address      = {London},
      publisher    = {BMJ Publishing Group},
      reportid     = {DKFZ-2017-00943},
      pages        = {939 - 954},
      year         = {2017},
      abstract     = {Bone morphogenetic protein (BMP)-9, a member of the
                      transforming growth factor-β family of cytokines, is
                      constitutively produced in the liver. Systemic levels act on
                      many organs and tissues including bone and endothelium, but
                      little is known about its hepatic functions in health and
                      disease.Levels of BMP-9 and its receptors were analysed in
                      primary liver cells. Direct effects of BMP-9 on hepatic
                      stellate cells (HSCs) and hepatocytes were studied in vitro,
                      and the role of BMP-9 was examined in acute and chronic
                      liver injury models in mice.Quiescent and activated HSCs
                      were identified as major BMP-9 producing liver cell type.
                      BMP-9 stimulation of cultured hepatocytes inhibited
                      proliferation, epithelial to mesenchymal transition and
                      preserved expression of important metabolic enzymes such as
                      cytochrome P450. Acute liver injury caused by partial
                      hepatectomy or single injections of carbon tetrachloride
                      (CCl4) or lipopolysaccharide (LPS) into mice resulted in
                      transient downregulation of hepatic BMP-9 mRNA expression.
                      Correspondingly, LPS stimulation led to downregulation of
                      BMP-9 expression in cultured HSCs. Application of BMP-9
                      after partial hepatectomy significantly enhanced liver
                      damage and disturbed the proliferative response. Chronic
                      liver damage in BMP-9-deficient mice or in mice adenovirally
                      overexpressing the selective BMP-9 antagonist activin-like
                      kinase 1-Fc resulted in reduced deposition of collagen and
                      subsequent fibrosis.Constitutive expression of low levels of
                      BMP-9 stabilises hepatocyte function in the healthy liver.
                      Upon HSC activation, endogenous BMP-9 levels increase in
                      vitro and in vivo and high levels of BMP-9 cause enhanced
                      damage upon acute or chronic injury.},
      cin          = {A190 / B200 / D120 / L101},
      ddc          = {610},
      cid          = {I:(DE-He78)A190-20160331 / I:(DE-He78)B200-20160331 /
                      I:(DE-He78)D120-20160331 / I:(DE-He78)L101-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28336518},
      doi          = {10.1136/gutjnl-2016-313314},
      url          = {https://inrepo02.dkfz.de/record/120514},
}