% IMPORTANT: The following is UTF-8 encoded. This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.
@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},
}