17 beta-Estradiol and steady-state concentrations of H2O2: antiapoptotic effect in endometrial cells from patients with endometriosis

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dc.contributor.author Andrade, Sheila Siqueira [UNIFESP]
dc.contributor.author Azevedo, Aline de Cássia [UNIFESP]
dc.contributor.author Monasterio, Izabel C. G. [UNIFESP]
dc.contributor.author Paredes-Gamero, Edgar Julian [UNIFESP]
dc.contributor.author Gonçalves, Giovana Aparecida [UNIFESP]
dc.contributor.author Bonetti, Tatiana Carvalho de Souza [UNIFESP]
dc.contributor.author Albertoni, Guilherme Ambrozio [UNIFESP]
dc.contributor.author Schor, Eduardo [UNIFESP]
dc.contributor.author Barreto, Jose A.
dc.contributor.author Oliva, Maria Luiza Vilela [UNIFESP]
dc.contributor.author Juliano, Luiz [UNIFESP]
dc.contributor.author Girão, Manoel João Batista Castello [UNIFESP]
dc.contributor.author Silva, Ismael Dale Cotrim Guerreiro da [UNIFESP]
dc.date.accessioned 2016-01-24T14:31:54Z
dc.date.available 2016-01-24T14:31:54Z
dc.date.issued 2013-07-01
dc.identifier http://dx.doi.org/10.1016/j.freeradbiomed.2013.01.034
dc.identifier.citation Free Radical Biology and Medicine. New York: Elsevier B.V., v. 60, p. 63-72, 2013.
dc.identifier.issn 0891-5849
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/36441
dc.description.abstract Increased levels of hydrogen peroxide (H2O2) can initiate protective responses to limit or repair oxidative damage. However, H2O2 signals also fine-tune responses to growth factors and cytokines controlling cell division, differentiation, and proliferation. Because 17 beta-estradiol (E-2) also plays important roles in these processes, and is considered a major risk factor in the development and progression of endometriosis, this study evaluated whether E-2 has an antiapoptotic effect on oxidative stress in endometrial cells in combination with steady-state H2O2 levels ([H2O2]ss). Endometrial stromal cells were prepared from the eutopic endometrium of 18 women with and without endometriosis to produce primary cells. These cells were stimulated with E-2 for 20 h, exposed to [H2O2]ss, and examined for cell viability, proliferation, and apoptosis. the endometrial cells from women with endometriosis maintained the steady state for 120 min at high H2O2 concentrations. When they were pretreated with E-2 and exposed to [H2O2]ss, a decrease in apoptosis level was observed compared to the control cells (p < 0.01). the endometrial cells from patients with endometriosis subjected to both E-2 and [H2O2]ss showed increased ERK phosphorylation. These findings suggested that H2O2 is a signaling molecule that downregulates apoptosis in endometrial cells, supporting the fact that endometriosis, albeit a benign disease, shares some features with cancer such as decreased catalase levels. These results link the E-2 effects on [H2O2]ss to resistance to apoptosis and progression of endometriosis. (C) 2013 Elsevier Inc. All rights reserved. en
dc.description.sponsorship Associacao Beneficente de Coleta de Sangue
dc.description.sponsorship Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorship Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.description.sponsorship Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.format.extent 63-72
dc.language.iso eng
dc.publisher Elsevier B.V.
dc.relation.ispartof Free Radical Biology and Medicine
dc.rights Acesso aberto
dc.subject Endometriosis en
dc.subject 17 beta-Estradiol en
dc.subject Hydrogen peroxide en
dc.subject Free radicals en
dc.title 17 beta-Estradiol and steady-state concentrations of H2O2: antiapoptotic effect in endometrial cells from patients with endometriosis en
dc.type Artigo
dc.rights.license http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.contributor.institution Charitable Assoc Blood Collect
dc.description.affiliation Universidade Federal de São Paulo, Dept Gynecol, BR-04044 São Paulo, Brazil
dc.description.affiliation Charitable Assoc Blood Collect, São Paulo, Brazil
dc.description.affiliation Universidade Federal de São Paulo, Dept Biochem, BR-04044 São Paulo, Brazil
dc.description.affiliation Universidade Federal de São Paulo, Dept Biophys, BR-04044 São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Dept Gynecol, BR-04044 São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Dept Biochem, BR-04044 São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Dept Biophys, BR-04044 São Paulo, Brazil
dc.identifier.file WOS000319486500009.pdf
dc.identifier.doi 10.1016/j.freeradbiomed.2013.01.034
dc.description.source Web of Science
dc.identifier.wos WOS:000319486500009



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