Expression and Signaling of G Protein-Coupled Estrogen Receptor 1 (GPER) in Rat Sertoli Cells

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dc.contributor.author Lucas, Thais F. G. [UNIFESP]
dc.contributor.author Royer, Carine [UNIFESP]
dc.contributor.author Siu, Erica R. [UNIFESP]
dc.contributor.author Lazari, Maria Fatima M. [UNIFESP]
dc.contributor.author Porto, Catarina S. [UNIFESP]
dc.date.accessioned 2016-01-24T14:05:14Z
dc.date.available 2016-01-24T14:05:14Z
dc.date.issued 2010-08-01
dc.identifier http://dx.doi.org/10.1095/biolreprod.110.084160
dc.identifier.citation Biology of Reproduction. Madison: Soc Study Reproduction, v. 83, n. 2, p. 307-317, 2010.
dc.identifier.issn 0006-3363
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/32743
dc.description.abstract The aim of the present study was to investigate the expression and signaling of the G protein-coupled estrogen receptor 1 (GPER) in cultured immature rat Sertoli cells-in which we have previously described the classical estrogen receptors (ESR1 and ESR2). Expression of GPER in cultured Sertoli cells from 15-day-old rats was detected by RT-PCR and immunoassays. Gper transcripts also were present in testes from 5-, 15-, and 120-day-old rats. Short-term treatment of Sertoli cells with 17beta-estradiol (E2), the GPER agonist G-1, or the ESR antagonist ICI 182,780 (ICI) rapidly activated MAPK3/1 (ERK1/2), even after down-regulation of ESR1 and ESR2, suggesting a role for GPER in the rapid E2 action in these cells. MAPK3/1 phosphorylation induced by ICI or G-1 was blocked by pertussis toxin, selective inhibitor of the SRC family of protein tyrosine kinases, metalloprotease inhibitor, MAP2K1/2 inhibitor, and epidermal growth factor receptor (EGFR) kinase inhibitor. Furthermore, E2, but not G-1, induced up-regulation of cyclin D1 in the Sertoli cells. This effect was blocked by ICI. E2 and G-1 decreased BAX and increased BCL2 expression and these effects were blocked by MAP2K1/2 inhibitor and EGFR kinase inhibitor. the pretreatment with ICI did not block the effect of E2. Taken together, these results indicate that in Sertoli cells 1) GPER-mediated MAPK3/1 activation occurs via EGFR transactivation through G protein beta gamma subunits that promote SRC-mediated metalloprotease-dependent release of EGFR ligands, which bind to EGFR and lead to MAPK3/1 phosphorylation; 2) E2-ESRs play a role in Sertoli cell proliferation; and 3) E2-GPER may regulate gene expression involved with apoptosis. ESR and GPER may mediate actions important for Sertoli cell function and maintenance of normal testis development and homeostasis. en
dc.description.sponsorship Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorship Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.format.extent 307-317
dc.language.iso eng
dc.publisher Soc Study Reproduction
dc.relation.ispartof Biology of Reproduction
dc.rights Acesso aberto
dc.subject estradiol en
dc.subject estradiol receptor en
dc.subject GPER en
dc.subject intracellular signaling en
dc.subject mechanisms of hormone action en
dc.subject Sertoli cells en
dc.subject signal transduction en
dc.title Expression and Signaling of G Protein-Coupled Estrogen Receptor 1 (GPER) in Rat Sertoli Cells en
dc.type Artigo
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.description.affiliation Universidade Federal de São Paulo, Sect Expt Endocrinol, Dept Pharmacol, Escola Paulista Med,INFAR, BR-04044020 São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Sect Expt Endocrinol, Dept Pharmacol, Escola Paulista Med,INFAR, BR-04044020 São Paulo, Brazil
dc.description.sponsorshipID FAPESP: 2004/01152-0
dc.description.sponsorshipID FAPESP: 2007/52471-6
dc.identifier.doi 10.1095/biolreprod.110.084160
dc.description.source Web of Science
dc.identifier.wos WOS:000280149800018



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