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HERO ID
6314784
Reference Type
Journal Article
Title
A nongenomic action of 17beta-estradiol as the mechanism underlying the acute suppression of secretion of luteinizing hormone
Author(s)
Arreguin-Arevalo, JA; Nett, TM
Year
2005
Is Peer Reviewed?
Yes
Journal
Biology of Reproduction
ISSN:
0006-3363
EISSN:
1529-7268
Volume
73
Issue
1
Page Numbers
115-122
Language
English
PMID
15772257
DOI
10.1095/biolreprod.105.040329
Web of Science Id
WOS:000229978700014
Abstract
The objective of the present study was to determine the ability of 17beta-estradiol (E(2)) and conjugated forms of E(2) (E(2) conjugated to BSA [E(2)-BSA] and a novel conjugate, E(2) conjugated to a small peptide [E(2)-PEP]) to prevent the GnRH-induced secretion of LH and to determine the role of estradiol receptors (ERs) and ER subtypes (ERalpha, also known as ESR1, and ERbeta, also known as ESR2) in the mediation of the acute action of E(2) in primary cultures of ovine pituitary cells. Preincubation of cells for 15 min with E(2), E(2)-BSA, or E(2)-PEP prevented the GnRH-induced secretion of LH (P < 0.01). Treatment of cells with nonestrogenic steroid hormones did not affect secretion of LH when given alone, nor did these steroids impair the E(2)-induced inhibition of LH secretion (P > 0.1). Likewise, treatment of cells with the ER-antagonists tamoxifen, hydroxytamoxifen, or ICI 182 780 did not affect (P > 0.1) secretion of LH when given alone but did prevent (P < 0.01) the inhibition by E(2) and the E(2)-conjugates on GnRH-induced secretion of LH. When cells were treated with subtype-selective ER agonists, the ERalpha agonist (propylpyrazole-triol), but not the ERbeta agonist (diarylpropionitrile), decreased (P < 0.01) the GnRH-induced secretion of LH. In conclusion, the rapidity by which E(2) prevented GnRH-induced release of LH in ovine pituitary cells suggests that this inhibition is mediated via a nongenomic action of E(2). The inhibition of GnRH-induced secretion of LH proved to be steroid specific and mediated by ERs. It may occur specifically through ERalpha. The fact that E(2)-BSA or E(2)-PEP mimicked the action of E(2) suggests that this effect was mediated by an ER associated with the plasma membrane.
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