Estrogen receptors mediate rapid activation of phospholipase C pathway in the rat endometrium

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dc.contributor.authorKonigame, Vivian Cristina
dc.contributor.authorSiu, Erica Rosanna [UNIFESP]
dc.contributor.authorRoyer, Carine [UNIFESP]
dc.contributor.authorLucas, Thais Fabiana Gameiro [UNIFESP]
dc.contributor.authorPorto, Catarina Segreti [UNIFESP]
dc.contributor.authorAbdalla, Fernando Mauricio Francis
dc.contributor.institutionInst Butantan
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2016-01-24T14:17:34Z
dc.date.available2016-01-24T14:17:34Z
dc.date.issued2011-12-20
dc.description.abstractThe aim of the present study was to investigate the activation of rapid signaling events by 17 beta-estradiol in the rat uterus. 17 beta-Estradiol induced a rapid increase of total [(3)H]-inositol phosphate accumulation in the whole uterus and endometrium, but not in the myometrium. the effect of 17 beta-estradiol in the endometrium was blocked by phospholipase C (PLC) inhibitor (1173122), estrogen receptors antagonist (ICI 182,780), exportin CRM1 inhibitor (leptomycin B) and selective inhibitor of the SRC family of protein tyrosine kinases (PP2). Furthermore, a selective agonist of ESR1 (PPT) and a selective agonist of GPER (G-1) also induced a rapid increase of total ((3)H]-inositol phosphate accumulation in the endometrium. the G-1 effects were blocked by GPER antagonist (G-15). 17 beta-Estradiol and G-1 promoted an additive effect on total [(3)H]-inositol phosphate accumulation. in conclusion, the present results indicate that a rapid activation of the PLC-mediated phosphoinositide hydrolysis occurred in the rat endometrium after 17 beta-estradiol stimulation, and this effect was mediated by ESR1 that underwent nuclear export after hormone stimulation, and that GPER activation may play an additive role for this response. These rapid actions might be one of the key steps that mediate the estrogen-dependent activation of cellular events in the endometrium. (C) 2011 Elsevier Inc. All rights reserved.en
dc.description.affiliationInst Butantan, Pharmacol Lab, BR-05503900 São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Sect Expt Endocrinol, Dept Pharmacol, Escola Paulista Med, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Sect Expt Endocrinol, Dept Pharmacol, Escola Paulista Med, São Paulo, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)pt
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)pt
dc.description.sponsorshipIDFAPESP: 06/53285-9pt
dc.format.extent1582-1589
dc.identifierhttps://dx.doi.org/10.1016/j.steroids.2011.09.013
dc.identifier.citationSteroids. New York: Elsevier B.V., v. 76, n. 14, p. 1582-1589, 2011.
dc.identifier.doi10.1016/j.steroids.2011.09.013
dc.identifier.issn0039-128X
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/34332
dc.identifier.wosWOS:000298273300010
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofSteroids
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.rights.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.subjectEndometriumen
dc.subject17 beta-Estradiolen
dc.subjectG-1en
dc.subjectInositol phosphateen
dc.subjectEstrogen receptorsen
dc.titleEstrogen receptors mediate rapid activation of phospholipase C pathway in the rat endometriumen
dc.typeinfo:eu-repo/semantics/article
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