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 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

Fingerprint

Dimerization
Gonadotropin-Releasing Hormone
Estrogen Receptor alpha
Estrogens
Membranes
LHRH Receptors
Feedback
Estrogen Receptor beta
Neurons
Estradiol

Keywords

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

ASJC Scopus subject areas

  • Endocrinology
  • Molecular Biology
  • Biochemistry

Cite this

GnRH agonist reduces estrogen receptor dimerization in GT1-7 cells : Evidence for cross-talk between membrane-initiated estrogen and GnRH signaling. / Chason, Rebecca J.; Kang, Jung Hoon; Gerkowicz, Sabrina A.; Dufau, Maria L.; Catt, Kevin J.; Segars, James.

In: Molecular and Cellular Endocrinology, Vol. 404, 05.03.2015, p. 67-74.

Research output: Contribution to journalArticle

Chason, Rebecca J. ; Kang, Jung Hoon ; Gerkowicz, Sabrina A. ; Dufau, Maria L. ; Catt, Kevin J. ; Segars, James. / GnRH agonist reduces estrogen receptor dimerization in GT1-7 cells : Evidence for cross-talk between membrane-initiated estrogen and GnRH signaling. In: Molecular and Cellular Endocrinology. 2015 ; Vol. 404. pp. 67-74.
@article{3d1dcfbd5c814d748a60a85d9494e88f,
title = "GnRH agonist reduces estrogen receptor dimerization in GT1-7 cells: Evidence for cross-talk between membrane-initiated estrogen and GnRH signaling",
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.",
keywords = "Estradiol, Estrogen receptor alpha, Estrogen receptor beta, GnRH receptor, GT1-7 cells, Non-classical estrogen signaling",
author = "Chason, {Rebecca J.} and Kang, {Jung Hoon} and Gerkowicz, {Sabrina A.} and Dufau, {Maria L.} and Catt, {Kevin J.} and James Segars",
year = "2015",
month = "3",
day = "5",
doi = "10.1016/j.mce.2015.01.023",
language = "English (US)",
volume = "404",
pages = "67--74",
journal = "Molecular and Cellular Endocrinology",
issn = "0303-7207",
publisher = "Elsevier Ireland Ltd",

}

TY - JOUR

T1 - GnRH agonist reduces estrogen receptor dimerization in GT1-7 cells

T2 - Evidence for cross-talk between membrane-initiated estrogen and GnRH signaling

AU - Chason, Rebecca J.

AU - Kang, Jung Hoon

AU - Gerkowicz, Sabrina A.

AU - Dufau, Maria L.

AU - Catt, Kevin J.

AU - Segars, James

PY - 2015/3/5

Y1 - 2015/3/5

N2 - 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.

AB - 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.

KW - Estradiol

KW - Estrogen receptor alpha

KW - Estrogen receptor beta

KW - GnRH receptor

KW - GT1-7 cells

KW - Non-classical estrogen signaling

UR - http://www.scopus.com/inward/record.url?scp=84922225761&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84922225761&partnerID=8YFLogxK

U2 - 10.1016/j.mce.2015.01.023

DO - 10.1016/j.mce.2015.01.023

M3 - Article

C2 - 25619861

AN - SCOPUS:84922225761

VL - 404

SP - 67

EP - 74

JO - Molecular and Cellular Endocrinology

JF - Molecular and Cellular Endocrinology

SN - 0303-7207

ER -