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@ARTICLE{Tisch:144870,
      author       = {N. Tisch and A. Freire-Valls and R. Yerbes and I. Paredes
                      and S. La Porta$^*$ and X. Wang and R. Martín-Pérez and L.
                      Castro and W. W. Wong and L. Coultas and B. Strilic and
                      H.-J. Gröne$^*$ and T. Hielscher$^*$ and C. Mogler and R.
                      Adams and P. Heiduschka and L. Claesson-Welsh and M. Mazzone
                      and A. López-Rivas and T. Schmidt and H. G. Augustin$^*$
                      and C. Ruiz de Almodovar},
      title        = {{C}aspase-8 modulates physiological and pathological
                      angiogenesis during retina development.},
      journal      = {The journal of clinical investigation},
      volume       = {129},
      number       = {12},
      issn         = {1558-8238},
      address      = {Ann Arbor, Mich.},
      publisher    = {ASCJ},
      reportid     = {DKFZ-2019-02294},
      pages        = {5092-5107},
      year         = {2019},
      note         = {2019 Dec 2;129(12):5092-5107},
      abstract     = {During developmental angiogenesis blood vessels grow and
                      remodel to ultimately build a hierarchical vascular network.
                      Whether and how cell death signaling molecules contribute to
                      blood vessel formation is still not well understood.
                      Caspase-8 (Casp-8), a key protease in the extrinsic cell
                      death-signaling pathway, regulates both cell death via
                      apoptosis and necroptosis. Here we show that expression of
                      Casp-8 in endothelial cells (ECs) was required for proper
                      postnatal retina angiogenesis. EC specific Casp-8 knockout
                      pups (Casp-8ECko) showed reduced retina angiogenesis, as the
                      loss of Casp-8 reduced EC proliferation, sprouting and
                      migration independent of its cell death function. Instead,
                      the loss of Casp-8 caused hyperactivation of p38
                      mitogen-activated protein kinase (MAPK) downstream of
                      receptor-interacting serine/threonine- protein kinase 3
                      (RIPK3) and destabilization of VE-cadherin at EC junctions.
                      In a mouse model of oxygen-induced retinopathy (OIR),
                      resembling retinopathy of prematurity (ROP), loss of Casp-8
                      in ECs was beneficial, as pathological neovascularization
                      was reduced in Casp-8ECko pups. Taken together, we describe
                      that Casp-8 acts in a cell-death independent manner in ECs
                      to regulate the formation of the retina vasculature and that
                      Casp-8 in ECs is mechanistically involved in the
                      pathophysiology of ROP.},
      cin          = {A190 / G130 / C060},
      ddc          = {610},
      cid          = {I:(DE-He78)A190-20160331 / I:(DE-He78)G130-20160331 /
                      I:(DE-He78)C060-20160331},
      pnm          = {319H - Addenda (POF3-319H)},
      pid          = {G:(DE-HGF)POF3-319H},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31454332},
      doi          = {10.1172/JCI122767},
      url          = {https://inrepo02.dkfz.de/record/144870},
}