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@ARTICLE{Zhang:131010,
      author       = {W. Zhang and M. Freichel and F. van der Hoeven$^*$ and P.
                      P. Nawroth and H. Katus and F. Kälble and E. Zitron and V.
                      Schwenger},
      title        = {{N}ovel {E}ndothelial {C}ell-{S}pecific {AQP}1 {K}nockout
                      {M}ice {C}onfirm the {C}rucial {R}ole of {E}ndothelial
                      {AQP}1 in {U}ltrafiltration during {P}eritoneal {D}ialysis.},
      journal      = {PLoS one},
      volume       = {11},
      number       = {1},
      issn         = {1932-6203},
      address      = {Lawrence, Kan.},
      publisher    = {PLoS},
      reportid     = {DKFZ-2017-06086},
      pages        = {e0145513 -},
      year         = {2016},
      abstract     = {The water channel aquaporin-1 (AQP1) mediates about $50\%$
                      ultrafiltration during a 2-hour hypertonic dwell in global
                      AQP1 knockout (AQP1-/-) mice. Although AQP1 is widely
                      expressed in various cell types including mesothelial cells,
                      the ultrafiltration has been assumed to be mediated via
                      endothelial AQP1 of the peritoneum. The partial embryonic
                      lethality and reduced body weight in AQP1-/- mice may
                      reflect potential confounding phenotypic effects evoked by
                      ubiquitous AQP1 deletion, which may interfere with
                      functional analysis of endothelial AQP1. Using a Cre/loxP
                      approach, we generated and characterised endothelial cell-
                      and time-specific AQP1 knockout (AQP1fl/fl; Cdh5-Cre+) mice.
                      Compared to controls, AQP1fl/fl; Cdh5-Cre+ mice showed no
                      difference in an initial clinical and biological analysis at
                      baseline, including body weight and survival. During a
                      1-hour $3.86\%$ mini-peritoneal equilibration test
                      (mini-PET), AQP1fl/fl; Cdh5-Cre+ mice exhibited strongly
                      decreased indices for AQP1-related transcellular water
                      transport $(43.0\%$ in net ultrafiltration, $93.0\%$ in
                      sodium sieving and $57.9\%$ in free water transport)
                      compared to controls. The transport rates for small solutes
                      of urea and glucose were not significantly altered. Our data
                      provide the first direct experimental evidence for the
                      functional relevance of endothelial AQP1 to the fluid
                      transport in peritoneal dialysis and thereby further
                      validate essential predictions of the three-pore model of
                      peritoneal transport.},
      keywords     = {Water (NLM Chemicals) / Aquaporin 1 (NLM Chemicals)},
      cin          = {W450},
      ddc          = {500},
      cid          = {I:(DE-He78)W450-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26760974},
      pmc          = {pmc:PMC4711985},
      doi          = {10.1371/journal.pone.0145513},
      url          = {https://inrepo02.dkfz.de/record/131010},
}