Tumor necrosis factor-α activates estrogen signaling pathways in endometrial epithelial cells via estrogen receptor α.

Détails

ID Serval
serval:BIB_6F66ED3EB771
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Tumor necrosis factor-α activates estrogen signaling pathways in endometrial epithelial cells via estrogen receptor α.
Périodique
Molecular and Cellular Endocrinology
Auteur(s)
Gori I., Pellegrini C., Staedler D., Russell R., Jan C., Canny G.O.
ISSN
1872-8057 (Electronic)
ISSN-L
0303-7207
Statut éditorial
Publié
Date de publication
2011
Volume
345
Numéro
1-2
Pages
27-37
Langue
anglais
Notes
Publication types: Journal Article
Publication Status: ppublish
Résumé
The pro-inflammatory cytokine TNF-α and the female hormone estrogen have been implicated in the pathophysiology of two common gynecological diseases, endometriosis and endometrial adenocarcinoma. Here we describe a novel capacity of TNF-α to activate ER signaling in endometrial epithelial cells. TNF-α induced luciferase expression in the absence and presence of estradiol and also augmented expression of the estrogen-regulated genes c-fos, GREB1, and progesterone receptor. Furthermore, TNF-α mediated ER transcriptional activity is dependent on the Extracellular Regulated Kinase (ERK) 1/2 pathway. Co-treatment with a pure ER antagonist resulted in an inhibition of this TNF-α-induced ERE luciferase activity and gene expression, demonstrating that this cytokine signals through ERs. Additional investigations confirmed that TNF-α acts specifically via ERα. Taken together, these data provide a rationale for the potential use of inhibitors of TNF-α and estrogen production/activity in combination for the treatment of endometrial pathologies.
Pubmed
Web of science
Création de la notice
15/08/2011 21:12
Dernière modification de la notice
20/10/2020 10:12
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