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

doi:10.1016/j.mce.2015.01.023

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 journal › Article › peer-review

10 Scopus citations

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 language	English (US)
Pages (from-to)	67-74
Number of pages	8
Journal	Molecular and Cellular Endocrinology
Volume	404
DOIs	https://doi.org/10.1016/j.mce.2015.01.023
State	Published - Mar 5 2015
Externally published	Yes

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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10.1016/j.mce.2015.01.023

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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, GT1-7 cells, GnRH receptor, 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 Segars, {James H.}",

note = "Funding Information: The authors thank Dr. Alan DeCherney for his support of the project, and Dr. Carlos Medina for approving and facilitating Dr. Gerkowicz's time at the NIH. This work was supported by the National Institutes of Health (Intramural Research Program of the NICHD), Grants Z01-HD 008737 (Dr. James Segars), Z01-HD 00184 (Dr. Kevin Catt) and ZIA-HD 000150-39 (Dr. Maria Dufau). Publisher Copyright: {\textcopyright} 2015.",

year = "2015",

month = mar,

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",

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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 H.

N1 - Funding Information: The authors thank Dr. Alan DeCherney for his support of the project, and Dr. Carlos Medina for approving and facilitating Dr. Gerkowicz's time at the NIH. This work was supported by the National Institutes of Health (Intramural Research Program of the NICHD), Grants Z01-HD 008737 (Dr. James Segars), Z01-HD 00184 (Dr. Kevin Catt) and ZIA-HD 000150-39 (Dr. Maria Dufau). Publisher Copyright: © 2015.

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 - GT1-7 cells

KW - GnRH receptor

KW - Non-classical estrogen signaling

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JO - Molecular and Cellular Endocrinology

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ER -

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

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Keywords

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