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

Details

Serval ID
serval:BIB_96B00DFFAF04
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
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
Journal
Neuroendocrinology
Author(s)
Kehrer  P., Turnill  D., Dayer  J. M., Muller  A. F., Gaillard  R. C.
ISSN
0028-3835 (Print)
Publication state
Published
Issued date
08/1988
Volume
48
Number
2
Pages
160-6
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Aug
Abstract
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)
Keywords
Adrenocorticotropic Hormone/*secretion Animals Cells, Cultured Cyclic AMP/*physiology Dexamethasone/pharmacology Dinoprostone/*physiology Female Growth Hormone/pharmacology Interferon Type I/*pharmacology Interferon Type I, Recombinant/*pharmacology Kinetics Luteinizing Hormone/secretion Pituitary Gland, Anterior/drug effects/*secretion Rats Rats, Inbred Strains Recombinant Proteins/*pharmacology Reference Values Tumor Necrosis Factor-alpha/*pharmacology
Pubmed
Web of science
Create date
15/02/2008 17:58
Last modification date
20/08/2019 15:58
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