Titre
Human recombinant interleukin-1 beta and -alpha, but not recombinant tumor necrosis factor alpha stimulate ACTH release from rat anterior pituitary cells in vitro in a prostaglandin E2 and cAMP independent manner
Type
article
Institution
UNIL/CHUV/Unisanté + institutions partenaires
Périodique
Auteur(s)
Kehrer, P.
Auteure/Auteur
Turnill, D.
Auteure/Auteur
Dayer, J. M.
Auteure/Auteur
Muller, A. F.
Auteure/Auteur
Gaillard, R. C.
Auteure/Auteur
Liens vers les personnes
rgaillar
Liens vers les unités
ISSN
0028-3835
Statut éditorial
Publié
Date de publication
1988-08
Volume
48
Numéro
2
Première page
160
Dernière page/numéro d’article
6
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Aug
Research Support, Non-U.S. Gov't --- Old month value: Aug
Résumé
The pituitary-adrenal axis is known to be stimulated during the acute-phase response. As cytokines play a central role in mediating the constellation of host response occurring during the acute-phase response it was of interest to assess the ability of cytokines to stimulate ACTH secretion from normal pituitary cells in culture. We used human recombinant interleukin-1 beta and -alpha (hrIL1 beta, hrIL1 alpha) and human recombinant tumor necrosis factor alpha (hrTNF alpha) to analyze the ability of these cytokines to induce ACTH secretion from normal rat anterior pituitary cells in culture. We also investigated the possible roles of prostaglandin E2 (PGE2) and cAMP in the cellular transduction mechanism. After 3 days of incubation primary cultures of rat anterior pituitary cells were stimulated for 24 h with either hrIL1 beta, hrIL1 alpha or hrTNF alpha alone or with the addition of dexamethasone or indomethacin. The culture media were analyzed for ACTH, PGE2 and cAMP content. At doses ranging from 0.03 to 30 nM, hrIL1 beta stimulated the release of ACTH and PGE2 in a dose-dependent manner. In contrast, at doses ranging from 3 to 60 nM, hrTNF alpha was unable to stimulate ACTH secretion although it stimulated PGE2 synthesis. Time-course experiments demonstrated that hrIL1 beta (3 nM) stimulates ACTH production over a period of 8, 16 and 24 h, but not after a period of 4 h. In these experiments, hrIL1 beta failed to cause any change in the secretions of growth hormone and luteinizing hormone.(ABSTRACT TRUNCATED AT 250 WORDS)
Sujets
PID Serval
serval:BIB_96B00DFFAF04
PMID
Date de création
2008-02-15T15:58:12.633Z
Date de création dans IRIS
2025-05-21T00:35:58Z