17β-Estradiol activates rapid signaling pathways involved in rat pachytene spermatocytes apoptosis through GPR30 and ERα

Adele Chimento, Rosa Sirianni, Christelle Delalande, Dorothèe Silandre, Camille Bois, Sebastiano Andò, Marcello Maggiolini, Serge Carreau, Vincenzo Pezzi

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93 Scopus citations

Abstract

Aim of the present study was to investigate whether estrogens were able to directly activate rapid signaling pathways controlling spermatogenesis in rat pachytene spermatocytes (PS). Classically, estrogens act by binding to estrogen receptors (ERs) α and β Recently, it has been demonstrated that rapid estrogen action can also be activated through the G-protein-coupled receptor (GPR)-30. Herein, we demonstrated that rat PS express ERα, ERβ and GPR30. Treatment of PS with estradiol (E2), the selective GPR30 agonist G1 and the selective ERα agonist PPT determined activation of ERK1/2 which are part of GPR30 signaling cascade. ERK1/2 activation in response to E2 and G1 was correlated to an increased phosphorylation of c-Jun. All treatments failed to induce these responses in the presence of EGFR inhibitor AG1478, ERK inhibitor PD98059 and ER inhibitor ICI182780. mRNA expression of cell cycle regulators cyclin A1 and B1 was downregulated by E2 and G1 while an up-regulation of proapoptotic factor Bax was observed in the same conditions. These data demonstrate that E2, working through both ERα and/or GPR30, activates in PS the rapid EGFR/ERK/c-Jun pathway, modulating the expression of genes involved in the balance between cellular proliferation and apoptosis.

Original languageEnglish (US)
Pages (from-to)136-144
Number of pages9
JournalMolecular and Cellular Endocrinology
Volume320
Issue number1-2
DOIs
Publication statusPublished - May 2010

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Keywords

  • Apoptosis
  • Estrogen
  • GPR30
  • Rat
  • Spermatocytes

ASJC Scopus subject areas

  • Endocrinology
  • Molecular Biology
  • Biochemistry

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