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@ARTICLE{Schneller:142851,
      author       = {D. Schneller$^*$ and R. Hofer-Warbinek and C. Sturtzel and
                      K. Lipnik and B. Gencelli and M. Seltenhammer and M. Wen and
                      J. Testori and M. Bilban and A. Borowski and M. Windwarder
                      and S. Kapel$^*$ and E. Besemfelder$^*$ and P. Cejka and A.
                      Habertheuer and B. Schlechta and O. Majdic and F. Altmann
                      and A. Kocher and H. Augustin$^*$ and W. Luttmann and E.
                      Hofer},
      title        = {{C}ytokine-{L}ike 1 {I}s a {N}ovel {P}roangiogenic {F}actor
                      {S}ecreted by and {M}ediating {F}unctions of {E}ndothelial
                      {P}rogenitor {C}ells.},
      journal      = {Circulation research},
      volume       = {124},
      number       = {2},
      issn         = {1524-4571},
      address      = {New York, NY},
      publisher    = {Assoc.},
      reportid     = {DKFZ-2019-00481},
      pages        = {243 - 255},
      year         = {2019},
      note         = {DKFZ-ZMBH Alliance},
      abstract     = {Endothelial colony forming cells (ECFCs) or late blood
                      outgrowth endothelial cells can be isolated from human cord
                      or peripheral blood, display properties of endothelial
                      progenitors, home into ischemic tissues and support
                      neovascularization in ischemic disease models.To assess the
                      functions of CYTL1 (cytokine-like 1), a factor we found
                      preferentially produced by ECFCs, in regard of vessel
                      formation.We show by transcriptomic analysis that ECFCs are
                      distinguished from endothelial cells of the vessel wall by
                      production of high amounts of CYTL1. Modulation of
                      expression demonstrates that the factor confers increased
                      angiogenic sprouting capabilities to ECFCs and can also
                      trigger sprouting of mature endothelial cells. The data
                      further display that CYTL1 can be induced by hypoxia and
                      that it functions largely independent of VEGF-A (vascular
                      endothelial growth factor-A). By recombinant production of
                      CYTL1 we confirm that the peptide is indeed a strong
                      proangiogenic factor and induces sprouting in cellular
                      assays and functional vessel formation in animal models
                      comparable to VEGF-A. Mass spectroscopy corroborates that
                      CYTL1 is specifically O-glycosylated on 2 neighboring
                      threonines in the C-terminal part and this modification is
                      important for its proangiogenic bioactivity. Further
                      analyses show that the factor does not upregulate
                      proinflammatory genes and strongly induces several
                      metallothionein genes encoding anti-inflammatory and
                      antiapoptotic proteins.We conclude that CYTL1 can mediate
                      proangiogenic functions ascribed to endothelial progenitors
                      such as ECFCs in vivo and may be a candidate to support
                      vessel formation and tissue regeneration in ischemic
                      pathologies.},
      cin          = {A100 / A190},
      ddc          = {610},
      cid          = {I:(DE-He78)A100-20160331 / I:(DE-He78)A190-20160331},
      pnm          = {321 - Basic Concepts (POF3-321)},
      pid          = {G:(DE-HGF)POF3-321},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30582450},
      doi          = {10.1161/CIRCRESAHA.118.313645},
      url          = {https://inrepo02.dkfz.de/record/142851},
}