English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

Long non-coding RNA PCAT19 safeguards DNA in quiescent endothelial cells by preventing uncontrolled phosphorylation of RPA2.

MPS-Authors
/persons/resource/persons251645

Oo,  James A
IMPRS, Max Planck Institute for Heart and Lung Research, Max Planck Society;

/persons/resource/persons251610

Warwick,  Timothy
IMPRS, Max Planck Institute for Heart and Lung Research, Max Planck Society;

/persons/resource/persons269910

Haydar,  Shaza
IMPRS, Max Planck Institute for Heart and Lung Research, Max Planck Society;

/persons/resource/persons224128

Gunther,  Stefan
Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, Max Planck Society;

External Resource
No external resources are shared
Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

Oo, J. A., Palfi, K., Warwick, T., Wittig, I., Prieto-Garcia, C., Matkovic, V., et al. (2022). Long non-coding RNA PCAT19 safeguards DNA in quiescent endothelial cells by preventing uncontrolled phosphorylation of RPA2. Cell reports, 41(7). doi:10.1016/j.celrep.2022.111670.


Cite as: https://hdl.handle.net/21.11116/0000-000B-92BA-E
Abstract
In healthy vessels, endothelial cells maintain a stable, differentiated, and growth-arrested phenotype for years. Upon injury, a rapid phenotypic switch facilitates proliferation to restore tissue perfusion. Here we report the identification of the endothelial cell-enriched long non-coding RNA (lncRNA) PCAT19, which contributes to the proliferative switch and acts as a safeguard for the endothelial genome. PCAT19 is enriched in confluent, quiescent endothelial cells and binds to the full replication protein A (RPA) complex in a DNA damage- and cell-cycle-related manner. Our results suggest that PCAT19 limits the phosphorylation of RPA2, primarily on the serine 33 (S33) residue, and thereby facilitates an appropriate DNA damage response while slowing cell cycle progression. Reduction in PCAT19 levels in response to either loss of cell contacts or knockdown promotes endothelial proliferation and angiogenesis. Collectively, PCAT19 acts as a dynamic guardian of the endothelial genome and facilitates rapid switching from quiescence to proliferation. Copyright © 2022 The Author(s). Published by Elsevier Inc. All rights reserved.