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@ARTICLE{Boos:212492,
      author       = {F. Boos and J. A. Oo and T. Warwick and S. Günther and J.
                      Izquierdo Ponce and M. Lopez and D. Rafii and G. Buchmann
                      and M. D. Pham and Z. S. Msheik and T. Li and S. Seredinski
                      and S. Haydar and S. Kashefiolasl and K. H. Plate$^*$ and R.
                      Behr and M. Mietsch and J. Krishnan and S. S. Pullamsetti
                      and S.-I. Bibli and R. Hinkel and A. H. Baker and R. A. Boon
                      and M. H. Schulz and I. Wittig and F. J. Miller and R. P.
                      Brandes and M. S. Leisegang},
      title        = {{T}he endothelial-enriched lnc{RNA} {LINC}00607 mediates
                      angiogenic function.},
      journal      = {Basic research in cardiology},
      volume       = {118},
      number       = {1},
      issn         = {0003-9217},
      address      = {Heidelberg},
      publisher    = {Springer},
      reportid     = {DKFZ-2023-00193},
      pages        = {5},
      year         = {2023},
      abstract     = {Long non-coding RNAs (lncRNAs) can act as regulatory RNAs
                      which, by altering the expression of target genes, impact on
                      the cellular phenotype and cardiovascular disease
                      development. Endothelial lncRNAs and their vascular
                      functions are largely undefined. Deep RNA-Seq and FANTOM5
                      CAGE analysis revealed the lncRNA LINC00607 to be highly
                      enriched in human endothelial cells. LINC00607 was induced
                      in response to hypoxia, arteriosclerosis regression in
                      non-human primates, post-atherosclerotic cultured
                      endothelial cells from patients and also in response to
                      propranolol used to induce regression of human arteriovenous
                      malformations. siRNA knockdown or CRISPR/Cas9 knockout of
                      LINC00607 attenuated VEGF-A-induced angiogenic sprouting.
                      LINC00607 knockout in endothelial cells also integrated less
                      into newly formed vascular networks in an in vivo assay in
                      SCID mice. Overexpression of LINC00607 in CRISPR knockout
                      cells restored normal endothelial function. RNA- and
                      ATAC-Seq after LINC00607 knockout revealed changes in the
                      transcription of endothelial gene sets linked to the
                      endothelial phenotype and in chromatin accessibility around
                      ERG-binding sites. Mechanistically, LINC00607 interacted
                      with the SWI/SNF chromatin remodeling protein BRG1.
                      CRISPR/Cas9-mediated knockout of BRG1 in HUVEC followed by
                      $CUT\&RUN$ revealed that BRG1 is required to secure a stable
                      chromatin state, mainly on ERG-binding sites. In conclusion,
                      LINC00607 is an endothelial-enriched lncRNA that maintains
                      ERG target gene transcription by interacting with the
                      chromatin remodeler BRG1 to ultimately mediate
                      angiogenesis.},
      keywords     = {BRG1 (Other) / ERG (Other) / Endothelial cell (Other) /
                      Gene regulation (Other) / Hypoxia (Other) / Long non-coding
                      RNA (Other)},
      cin          = {FM01},
      ddc          = {610},
      cid          = {I:(DE-He78)FM01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36700983},
      doi          = {10.1007/s00395-023-00978-3},
      url          = {https://inrepo02.dkfz.de/record/212492},
}