The endothelial-enriched lncRNA LINC00607 mediates angiogenic function.
BRG1
ERG
Endothelial cell
Gene regulation
Hypoxia
Long non-coding RNA
Journal
Basic research in cardiology
ISSN: 1435-1803
Titre abrégé: Basic Res Cardiol
Pays: Germany
ID NLM: 0360342
Informations de publication
Date de publication:
26 01 2023
26 01 2023
Historique:
received:
04
05
2022
accepted:
09
01
2023
revised:
09
01
2023
entrez:
26
1
2023
pubmed:
27
1
2023
medline:
31
1
2023
Statut:
epublish
Résumé
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.
Identifiants
pubmed: 36700983
doi: 10.1007/s00395-023-00978-3
pii: 10.1007/s00395-023-00978-3
pmc: PMC9879848
doi:
Substances chimiques
Chromatin
0
DNA Helicases
EC 3.6.4.-
Nuclear Proteins
0
RNA, Long Noncoding
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
5Subventions
Organisme : BLRD VA
ID : I01 BX001729
Pays : United States
Organisme : British Heart Foundation
ID : RG/20/5/34796
Pays : United Kingdom
Organisme : British Heart Foundation
ID : SP/F/22/150029
Pays : United Kingdom
Organisme : British Heart Foundation
ID : PG/20/10347
Pays : United Kingdom
Organisme : British Heart Foundation
ID : ReGenLnc
Pays : United Kingdom
Organisme : British Heart Foundation
ID : CH/11/2/28733
Pays : United Kingdom
Informations de copyright
© 2023. The Author(s).
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