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@ARTICLE{Gehrs:297968,
      author       = {S. Gehrs$^*$ and M. V. Jakab$^*$ and E. Gutjahr and Z. Gu
                      and D. Weichenhan$^*$ and J.-P. Mallm$^*$ and C. Mogler and
                      M. Schlesner and C. Plass$^*$ and K. Schlereth$^*$ and H.
                      Augustin$^*$},
      title        = {{T}he spatial zonation of the murine placental vasculature
                      is specified by epigenetic mechanisms.},
      journal      = {Developmental cell},
      volume       = {60},
      number       = {10},
      issn         = {1534-5807},
      address      = {Cambridge, Mass.},
      publisher    = {Cell Press},
      reportid     = {DKFZ-2025-00145},
      pages        = {1467-1482.e8},
      year         = {2025},
      note         = {#EA:A190#LA:A190# / 2025 May 19;60(10):1467-1482.e8},
      abstract     = {The labyrinthian fetoplacental capillary network is vital
                      for proper nourishment of the developing embryo. Dysfunction
                      of the maternal-fetal circulation is a primary cause of
                      placental insufficiency. Here, we show that the spatial
                      zonation of the murine placental labyrinth vasculature is
                      controlled by flow-regulated epigenetic mechanisms.
                      Spatiotemporal transcriptomic profiling identified a gradual
                      change in the expression of epigenetic enzymes, including
                      the de novo DNA methyltransferase 3a (DNMT3A). Loss of
                      Dnmt3a resulted in DNA hypomethylation and perturbation of
                      zonated placental gene expression. The resulting global DNA
                      hypomethylation impaired the angiogenic capacity of
                      endothelial cells. Global or endothelium-predominant
                      deletion of Dnmt3a resulted in impaired placental
                      vascularization and fetal growth retardation (FGR). Human
                      placental endothelial gene expression profiling associated
                      preeclampsia with reduced DNMT3A expression. Collectively,
                      our study identified DMNT3A as critical methylome-regulator
                      of placental endothelial gene expression and function with
                      clinical implications for placental dysfunction, as it
                      occurs during preeclampsia or FGR.},
      keywords     = {DNA methylation (Other) / DNMT3A (Other) / angiogenesis
                      (Other) / epigenetic regulation (Other) / growth retardation
                      (Other) / placental endothelium (Other) / spatial zonation
                      (Other)},
      cin          = {A190 / B370 / B066},
      ddc          = {610},
      cid          = {I:(DE-He78)A190-20160331 / I:(DE-He78)B370-20160331 /
                      I:(DE-He78)B066-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39814015},
      doi          = {10.1016/j.devcel.2024.12.037},
      url          = {https://inrepo02.dkfz.de/record/297968},
}