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

Rebecca J. Chason, Jung Hoon Kang, Sabrina A. Gerkowicz, Maria L. Dufau, Kevin J. Catt, James H. Segars

Research output: Contribution to journalArticle

Abstract

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 cells treated with E2. In BRET1 experiments, ERα-ERα dimerization was suppressed in GT1-7 cells treated with GnRH agonist (p < 0.05). There was no evidence of direct interaction between ERs and GnRH-R. This study provides the first evidence of reduced ERα homodimerization by GnRH agonist. Collectively, these findings demonstrate significant cross-talk between membrane-initiated GnRH and E2 signaling in GT1-7 cells.

Original languageEnglish (US)
Pages (from-to)67-74
Number of pages8
JournalMolecular and Cellular Endocrinology
Volume404
DOIs
StatePublished - Mar 5 2015
Externally publishedYes

Keywords

  • Estradiol
  • Estrogen receptor alpha
  • Estrogen receptor beta
  • GT1-7 cells
  • GnRH receptor
  • Non-classical estrogen signaling

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Endocrinology

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