Abstract:
:Vascular permeability is frequently associated with inflammation and is triggered by a cohort of secreted permeability factors such as vascular endothelial growth factor (VEGF). Here, we show that the physiological vascular permeability that precedes implantation is directly controlled by progesterone receptor (PR) and is independent of VEGF. Global or endothelial-specific deletion of PR blocks physiological vascular permeability in the uterus, whereas misexpression of PR in the endothelium of other organs results in ectopic vascular leakage. Integration of an endothelial genome-wide transcriptional profile with chromatin immunoprecipitation sequencing revealed that PR induces an NR4A1 (Nur77/TR3)-dependent transcriptional program that broadly regulates vascular permeability in response to progesterone. Silencing of NR4A1 blocks PR-mediated permeability responses, indicating a direct link between PR and NR4A1. This program triggers concurrent suppression of several junctional proteins and leads to an effective, timely, and venous-specific regulation of vascular barrier function that is critical for embryo implantation.
journal_name
Celljournal_title
Cellauthors
Goddard LM,Murphy TJ,Org T,Enciso JM,Hashimoto-Partyka MK,Warren CM,Domigan CK,McDonald AI,He H,Sanchez LA,Allen NC,Orsenigo F,Chao LC,Dejana E,Tontonoz P,Mikkola HK,Iruela-Arispe MLdoi
10.1016/j.cell.2013.12.025subject
Has Abstractpub_date
2014-01-30 00:00:00pages
549-62issue
3eissn
0092-8674issn
1097-4172pii
S0092-8674(13)01594-8journal_volume
156pub_type
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