help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Thrailkill, K. M.
Right arrow Articles by Handwerger, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Thrailkill, K. M.
Right arrow Articles by Handwerger, S.

Endocrinology, Vol 123, 2930-2934, Copyright © 1988 by Endocrine Society


ARTICLES

Insulin-like growth factor I stimulates the synthesis and release of prolactin from human decidual cells

KM Thrailkill, A Golander, LE Underwood and S Handwerger
Department of Pediatrics, Duke University Medical Center, Durham, North Carolina 27710.

Recent studies suggest a role for insulin-like growth factor I (IGF-I) in the regulation of hormone release from placental, gonadal, and pituitary tissues. To examine whether IGF-I may also regulate the release of PRL from human decidual tissue, we have investigated the effect of recombinant human IGF-I on PRL release from monolayer cultures of human decidual cells exposed to IGF-I for up to 4 days. IGF- I (10-1000 ng/ml) stimulated a sustained dose-dependent increase in PRL release (half-maximal concentration, 25 ng/ml) beginning 48 h after initial exposure, but had no effect on the intracellular PRL content. The amounts of PRL released from maximally stimulated cultures on days 3 and 4 were 168 +/- 3% (mean +/- SEM) and 258 +/- 8% of control values, respectively. IGF-I-mediated effects were inhibited by cycloheximide (3.6 microM), suggesting that the increase in PRL was the result of newly synthesized hormone. The increase in PRL release was not due to a generalized effect on protein release, since IGF-I had no effect on the release of trichloroacetic acid-precipitable [35S]methionyl proteins. Radioligand competition studies indicate that the biological actions of IGF-I are mediated through interaction with the IGF-I receptor. Binding of radiolabeled IGF-I to decidual cells in suspension was specific, saturable, and displacable by unlabeled IGF-I, with a potency nearly 10 times greater than that of insulin. Furthermore, exposure of decidual cells to a monoclonal antibody to the IGF-I receptor (alpha-IR3) completely inhibited both IGF-I-mediated PRL release and specific binding of [125I]IGF-I to decidual cells. Since the actions of IGF-I occurred at physiological concentrations, these findings strongly support a role for IGF-I in the regulation of PRL secretion by human decidua.


This article has been cited by other articles:


Home page
Physiol. Rev.Home page
M. E. Freeman, B. Kanyicska, A. Lerant, and G. Nagy
Prolactin: Structure, Function, and Regulation of Secretion
Physiol Rev, October 1, 2000; 80(4): 1523 - 1631.
[Abstract] [Full Text] [PDF]


Home page
EndocrinologyHome page
S. Fruchtman, L. Jackson, and R. Borski
Insulin-Like Growth Factor I Disparately Regulates Prolactin and Growth Hormone Synthesis and Secretion: Studies Using the Teleost Pituitary Model
Endocrinology, August 1, 2000; 141(8): 2886 - 2894.
[Abstract] [Full Text] [PDF]


Home page
Reproductive SciencesHome page
L. J. Heffner, M. Kumari, and L. A. Benoit
Secretion of the Vasoactive Peptides, Endothelin, and Parathyroid Hormone-Related Peptide, by Decidual Explants From Pregnancies Complicated by Intrauterine Growth Restriction
Reproductive Sciences, September 1, 1999; 6(5): 273 - 277.
[Abstract] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1988 by The Endocrine Society