A Thromboxane A
angiogenesis
cyclooxygenase 2
endothelial cells
endothelial dysfunction
prostaglandin H2
thromboxan A2 receptor
Journal
Arteriosclerosis, thrombosis, and vascular biology
ISSN: 1524-4636
Titre abrégé: Arterioscler Thromb Vasc Biol
Pays: United States
ID NLM: 9505803
Informations de publication
Date de publication:
04 2022
04 2022
Historique:
pubmed:
4
3
2022
medline:
6
4
2022
entrez:
3
3
2022
Statut:
ppublish
Résumé
TP (thromboxane A We combined global transcriptome analysis, lipid mediator profiling, functional cell analyses, and in vivo angiogenesis assays to study the effects of endothelial TP overexpression or knockdown/knockout on the angiogenic capacity of endothelial cells in vitro and in vivo. Here we report that endothelial TP expression induces COX-2 (cyclooxygenase-2) in a G Our work uncovers a TP-driven COX-2-dependent feedback loop and important effector mechanisms that directly link TP upregulation to angiostatic TP signaling in endothelial cells. By these previously unrecognized mechanisms, pathological endothelial upregulation of the TP could directly foster endothelial dysfunction, microvascular rarefaction, and systemic hypertension even in the absence of exogenous sources of TP agonists.
Sections du résumé
BACKGROUND
TP (thromboxane A
METHODS
We combined global transcriptome analysis, lipid mediator profiling, functional cell analyses, and in vivo angiogenesis assays to study the effects of endothelial TP overexpression or knockdown/knockout on the angiogenic capacity of endothelial cells in vitro and in vivo.
RESULTS
Here we report that endothelial TP expression induces COX-2 (cyclooxygenase-2) in a G
CONCLUSIONS
Our work uncovers a TP-driven COX-2-dependent feedback loop and important effector mechanisms that directly link TP upregulation to angiostatic TP signaling in endothelial cells. By these previously unrecognized mechanisms, pathological endothelial upregulation of the TP could directly foster endothelial dysfunction, microvascular rarefaction, and systemic hypertension even in the absence of exogenous sources of TP agonists.
Identifiants
pubmed: 35236104
doi: 10.1161/ATVBAHA.121.317380
pmc: PMC8939709
doi:
Substances chimiques
Receptors, Thromboxane
0
Receptors, Thromboxane A2, Prostaglandin H2
0
Thromboxanes
0
Thromboxane A2
57576-52-0
Cyclooxygenase 2
EC 1.14.99.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
444-461Références
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