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Updated: Aug 17, 2026
Transgenic Rodent Assay for Quantifying Male Germ Cell Mutant Frequency
Published on: August 6, 2014
17-beta-estradiol elicits genomic and non-genomic responses in mouse male germ cells
Elena Vicini1, Maria Loiarro, Silvia Di Agostino
1Department of Histology and Medical Embriology, University of Rome La Sapienza, Rome, Italy.
Abstract:
Estrogens have been postulated to exert a detrimental effect on spermatogenesis in vivo. Since mouse male germ cells express estrogen receptors, we have investigated whether molecular pathways are activated by estrogen stimulation of these cells. Our results demonstrate that estrogen receptor beta is expressed in mitotic and meiotic male germ cells as well as in the spermatogonia derived GC-1 cell line. By using this cell line, we show that 17-beta-estradiol triggers activation of a transcriptional response that requires a functional estrogen receptor. Moreover, GC-1 cells respond to estrogens by transiently activating a signal transduction pathway that impinges on the mitogen-activated protein kinases (MAPK) ERK1 and -2. A similar dose-dependent transient activation of ERKs was also observed in primary mouse spermatocytes in culture. Activation by the estrogen was specific because other steroids such as progesterone and dihydrotestosterone were ineffective and because it could be blocked by the selective inhibitor of the ERK pathway and by competitive inhibitors of the estrogen receptor. Finally, we observed that 17-beta-estradiol does not affect spontaneous or induced apoptosis in cultured mouse spermatocytes, indicating that the apoptotic effects observed in vivo require additional testicular components.
Insights
Estrogen receptor beta is present in male germ cells. 17-beta-estradiol activates specific molecular pathways, including MAPK ERK1/2, in these cells without inducing apoptosis.
Area of Science:
- Reproductive Biology
- Endocrinology
- Molecular Biology
Background:
- Estrogens are suggested to negatively impact sperm production in vivo.
- Mouse male germ cells express estrogen receptors, prompting investigation into estrogen's molecular effects.
Purpose of the Study:
- To investigate molecular pathways activated by estrogen stimulation in mouse male germ cells.
- To determine if estrogen receptor beta (ERB) mediates these effects.
Main Methods:
- Utilized the GC-1 cell line, derived from spermatogonia, for in vitro studies.
- Administered 17-beta-estradiol and other steroids (progesterone, dihydrotestosterone).
- Assessed transcriptional response, estrogen receptor activation, and mitogen-activated protein kinase (MAPK) pathway signaling (ERK1/2).
- Examined apoptosis in cultured primary mouse spermatocytes.
Main Results:
- Estrogen receptor beta is expressed in mitotic/meiotic germ cells and the GC-1 cell line.
- 17-beta-estradiol activates a transcriptional response dependent on a functional estrogen receptor.
- Estrogen transiently activates the MAPK ERK1/2 pathway in GC-1 cells and primary spermatocytes.
- This activation is specific to estrogen and can be blocked by pathway inhibitors.
- 17-beta-estradiol does not affect apoptosis in cultured mouse spermatocytes.
Conclusions:
- Estrogen receptor beta mediates estrogenic signaling in male germ cells.
- Estrogen activates specific signal transduction pathways (MAPK) in these cells.
- In vitro studies suggest that in vivo apoptotic effects of estrogen require additional testicular factors.
