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@ARTICLE{Manavski:120577,
      author       = {Y. Manavski and T. Abel and J. Hu$^*$ and D. Kleinlützum
                      and C. J. Buchholz and C. Belz and H. Augustin$^*$ and R. A.
                      Boon and S. Dimmeler},
      title        = {{E}ndothelial transcription factor {KLF}2 negatively
                      regulates liver regeneration via induction of activin {A}.},
      journal      = {Proceedings of the National Academy of Sciences of the
                      United States of America},
      volume       = {114},
      number       = {15},
      issn         = {1091-6490},
      address      = {Washington, DC},
      publisher    = {National Acad. of Sciences},
      reportid     = {DKFZ-2017-01006},
      pages        = {3993 - 3998},
      year         = {2017},
      abstract     = {Endothelial cells (ECs) not only are important for oxygen
                      delivery but also act as a paracrine source for signals that
                      determine the balance between tissue regeneration and
                      fibrosis. Here we show that genetic inactivation of
                      flow-induced transcription factor Krüppel-like factor 2
                      (KLF2) in ECs results in reduced liver damage and
                      augmentation of hepatocyte proliferation after chronic liver
                      injury by treatment with carbon tetrachloride (CCl4). Serum
                      levels of GLDH3 and ALT were significantly reduced in
                      CCl4-treated EC-specific KLF2-deficient mice. In contrast,
                      transgenic overexpression of KLF2 in liver sinusoidal ECs
                      reduced hepatocyte proliferation. KLF2 induced activin A
                      expression and secretion from endothelial cells in vitro and
                      in vivo, which inhibited hepatocyte proliferation. However,
                      loss or gain of KLF2 expression did not change capillary
                      density and liver fibrosis, but significantly affected
                      hepatocyte proliferation. Taken together, the data
                      demonstrate that KLF2 induces an antiproliferative
                      secretome, including activin A, which attenuates liver
                      regeneration.},
      cin          = {A190},
      ddc          = {000},
      cid          = {I:(DE-He78)A190-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28348240},
      pmc          = {pmc:PMC5393189},
      doi          = {10.1073/pnas.1613392114},
      url          = {https://inrepo02.dkfz.de/record/120577},
}