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GnRH agonist reduces estrogen receptor dimerization in GT1-7 cells: evidence for cross-talk between membrane-initiated estrogen and GnRH signaling.

ABSTRACT: 17?-estradiol (E2), a key participant on the initiation of the LH surge, exerts both positive and negative feedback on GnRH neurons. We sought to investigate potential interactions between estrogen receptors alpha (ER?) and beta (ER?) and gonadotropin releasing hormone receptor (GnRH-R) in GT1-7 cells. Radioligand binding studies demonstrated a significant decrease in saturation E2 binding in cells treated with GnRH agonist. Conversely, there was a significant reduction in GnRH binding in GT1-7 cells treated with E2. In BRET(1) experiments, ER?-ER? dimerization was suppressed in GT1-7 cells treated with GnRH agonist (p?

SUBMITTER: Chason RJ 

PROVIDER: S-EPMC4590284 | biostudies-literature | 2015 Mar

REPOSITORIES: biostudies-literature

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GnRH agonist reduces estrogen receptor dimerization in GT1-7 cells: evidence for cross-talk between membrane-initiated estrogen and GnRH signaling.

Chason Rebecca J RJ   Kang Jung-Hoon JH   Gerkowicz Sabrina A SA   Dufau Maria L ML   Catt Kevin J KJ   Segars James H JH  

Molecular and cellular endocrinology 20150122

17β-estradiol (E2), a key participant on the initiation of the LH surge, exerts both positive and negative feedback on GnRH neurons. We sought to investigate potential interactions between estrogen receptors alpha (ERα) and beta (ERβ) and gonadotropin releasing hormone receptor (GnRH-R) in GT1-7 cells. Radioligand binding studies demonstrated a significant decrease in saturation E2 binding in cells treated with GnRH agonist. Conversely, there was a significant reduction in GnRH binding in GT1-7  ...[more]

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