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.

Vicini, E., Loiarro, M., Di Agostino, S., Corallini, S., Capolunghi, F., Carsetti, R., et al. (2006). 17-beta-estradiol elicits genomic and non-genomic responses in mouse male germ cells. JOURNAL OF CELLULAR PHYSIOLOGY, 206(1), 238-245 [10.1002/jcp.20454].

17-beta-estradiol elicits genomic and non-genomic responses in mouse male germ cells

GEREMIA, RAFFAELE;SETTE, CLAUDIO
2006

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.
Pubblicato
Rilevanza internazionale
Articolo
Sì, ma tipo non specificato
Settore BIO/16
English
Con Impact Factor ISI
Animals; Apoptosis; Enzyme Activation; Humans; Estrogen Receptor alpha; Mice; Extracellular Signal-Regulated MAP Kinases; Transcriptional Activation; Spermatocytes; Estradiol; Germ Cells; MAP Kinase Signaling System; Cells, Cultured; Genes, Reporter; Male; Cell Line; Estrogen Receptor beta
Vicini, E., Loiarro, M., Di Agostino, S., Corallini, S., Capolunghi, F., Carsetti, R., et al. (2006). 17-beta-estradiol elicits genomic and non-genomic responses in mouse male germ cells. JOURNAL OF CELLULAR PHYSIOLOGY, 206(1), 238-245 [10.1002/jcp.20454].
Vicini, E; Loiarro, M; Di Agostino, S; Corallini, S; Capolunghi, F; Carsetti, R; Chieffi, P; Geremia, R; Stefanini, M; Sette, C
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/43527
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