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@ARTICLE{Schlereth:134840,
      author       = {K. Schlereth$^*$ and D. Weichenhan$^*$ and T. Bauer$^*$ and
                      T. Heumann$^*$ and E. Giannakouri$^*$ and D. Lipka$^*$ and
                      S. Jaeger and M. Schlesner$^*$ and P. Aloy and R. Eils$^*$
                      and C. Plass$^*$ and H. G. Augustin$^*$},
      title        = {{T}he transcriptomic and epigenetic map of vascular
                      quiescence in the continuous lung endothelium.},
      journal      = {eLife},
      volume       = {7},
      issn         = {2050-084X},
      address      = {Cambridge},
      publisher    = {eLife Sciences Publications},
      reportid     = {DKFZ-2018-00630},
      pages        = {e34423},
      year         = {2018},
      note         = {DKFZ-ZMBH-Allianz Plass C*, Augustin HG*, (*= Contributed
                      equally)},
      abstract     = {Maintenance of a quiescent and
                      organotypically-differentiated layer of blood vessel-lining
                      endothelial cells (EC) is vital for human health. Yet, the
                      molecular mechanisms of vascular quiescence remain largely
                      elusive. Here we identify the genome-wide transcriptomic
                      program controlling the acquisition of quiescence by
                      comparing lung EC of infant and adult mice, revealing a
                      prominent regulation of TGFß family members. These
                      transcriptomic changes are distinctly accompanied by
                      epigenetic modifications, measured at single CpG resolution.
                      Gain of DNA methylation affects developmental pathways,
                      including NOTCH signaling. Conversely, loss of DNA
                      methylation preferentially occurs in intragenic clusters
                      affecting intronic enhancer regions of genes involved in
                      TGFβ family signaling. Functional experiments
                      prototypically validated the strongly epigenetically
                      regulated inhibitors of TGFβ family signaling SMAD6 and
                      SMAD7 as regulators of EC quiescence. These data establish
                      the transcriptional and epigenetic landscape of vascular
                      quiescence that will serve as a foundation for further
                      mechanistic studies of vascular homeostasis and
                      disease-associated activation.},
      cin          = {A190 / C010 / B080 / B240 / L101},
      ddc          = {500},
      cid          = {I:(DE-He78)A190-20160331 / I:(DE-He78)C010-20160331 /
                      I:(DE-He78)B080-20160331 / I:(DE-He78)B240-20160331 /
                      I:(DE-He78)L101-20160331},
      pnm          = {321 - Basic Concepts (POF3-321)},
      pid          = {G:(DE-HGF)POF3-321},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29749927},
      pmc          = {pmc:PMC5947988},
      doi          = {10.7554/eLife.34423},
      url          = {https://inrepo02.dkfz.de/record/134840},
}