17 beta-Estradiol and steady-state concentrations of H2O2: antiapoptotic effect in endometrial cells from patients with endometriosis
Autor(a) principal: | |
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Data de Publicação: | 2013 |
Outros Autores: | , , , , , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://repositorio.unifesp.br/handle/11600/36441 http://dx.doi.org/10.1016/j.freeradbiomed.2013.01.034 |
Resumo: | 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. |
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Andrade, Sheila Siqueira [UNIFESP]Azevedo, Aline de Cássia [UNIFESP]Monasterio, Izabel C. G. [UNIFESP]Paredes-Gamero, Edgar Julian [UNIFESP]Gonçalves, Giovana Aparecida [UNIFESP]Bonetti, Tatiana Carvalho de Souza [UNIFESP]Albertoni, Guilherme Ambrozio [UNIFESP]Schor, Eduardo [UNIFESP]Barreto, Jose A.Oliva, Maria Luiza Vilela [UNIFESP]Juliano, Luiz [UNIFESP]Girão, Manoel João Batista Castello [UNIFESP]Silva, Ismael Dale Cotrim Guerreiro da [UNIFESP]Universidade Federal de São Paulo (UNIFESP)Charitable Assoc Blood Collect2016-01-24T14:31:54Z2016-01-24T14:31:54Z2013-07-01Free Radical Biology and Medicine. New York: Elsevier B.V., v. 60, p. 63-72, 2013.0891-5849http://repositorio.unifesp.br/handle/11600/36441http://dx.doi.org/10.1016/j.freeradbiomed.2013.01.034WOS000319486500009.pdf10.1016/j.freeradbiomed.2013.01.034WOS:000319486500009Increased 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.Associacao Beneficente de Coleta de SangueFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Universidade Federal de São Paulo, Dept Gynecol, BR-04044 São Paulo, BrazilCharitable Assoc Blood Collect, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Biochem, BR-04044 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Biophys, BR-04044 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Gynecol, BR-04044 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Biochem, BR-04044 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Biophys, BR-04044 São Paulo, BrazilWeb of Science63-72engElsevier B.V.Free Radical Biology and Medicinehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policyinfo:eu-repo/semantics/openAccessEndometriosis17 beta-EstradiolHydrogen peroxideFree radicals17 beta-Estradiol and steady-state concentrations of H2O2: antiapoptotic effect in endometrial cells from patients with endometriosisinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlereponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESPORIGINALWOS000319486500009.pdfapplication/pdf593278${dspace.ui.url}/bitstream/11600/36441/1/WOS000319486500009.pdfe965c8e1426ca3daacd83b64d71fe71aMD51open accessTEXTWOS000319486500009.pdf.txtWOS000319486500009.pdf.txtExtracted texttext/plain57162${dspace.ui.url}/bitstream/11600/36441/2/WOS000319486500009.pdf.txtca78fbd09574b7195604e16b3ca57ffdMD52open access11600/364412022-06-02 09:02:10.35open accessoai:repositorio.unifesp.br:11600/36441Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652023-05-25T12:13:10.961263Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.en.fl_str_mv |
17 beta-Estradiol and steady-state concentrations of H2O2: antiapoptotic effect in endometrial cells from patients with endometriosis |
title |
17 beta-Estradiol and steady-state concentrations of H2O2: antiapoptotic effect in endometrial cells from patients with endometriosis |
spellingShingle |
17 beta-Estradiol and steady-state concentrations of H2O2: antiapoptotic effect in endometrial cells from patients with endometriosis Andrade, Sheila Siqueira [UNIFESP] Endometriosis 17 beta-Estradiol Hydrogen peroxide Free radicals |
title_short |
17 beta-Estradiol and steady-state concentrations of H2O2: antiapoptotic effect in endometrial cells from patients with endometriosis |
title_full |
17 beta-Estradiol and steady-state concentrations of H2O2: antiapoptotic effect in endometrial cells from patients with endometriosis |
title_fullStr |
17 beta-Estradiol and steady-state concentrations of H2O2: antiapoptotic effect in endometrial cells from patients with endometriosis |
title_full_unstemmed |
17 beta-Estradiol and steady-state concentrations of H2O2: antiapoptotic effect in endometrial cells from patients with endometriosis |
title_sort |
17 beta-Estradiol and steady-state concentrations of H2O2: antiapoptotic effect in endometrial cells from patients with endometriosis |
author |
Andrade, Sheila Siqueira [UNIFESP] |
author_facet |
Andrade, Sheila Siqueira [UNIFESP] Azevedo, Aline de Cássia [UNIFESP] Monasterio, Izabel C. G. [UNIFESP] Paredes-Gamero, Edgar Julian [UNIFESP] Gonçalves, Giovana Aparecida [UNIFESP] Bonetti, Tatiana Carvalho de Souza [UNIFESP] Albertoni, Guilherme Ambrozio [UNIFESP] Schor, Eduardo [UNIFESP] Barreto, Jose A. Oliva, Maria Luiza Vilela [UNIFESP] Juliano, Luiz [UNIFESP] Girão, Manoel João Batista Castello [UNIFESP] Silva, Ismael Dale Cotrim Guerreiro da [UNIFESP] |
author_role |
author |
author2 |
Azevedo, Aline de Cássia [UNIFESP] Monasterio, Izabel C. G. [UNIFESP] Paredes-Gamero, Edgar Julian [UNIFESP] Gonçalves, Giovana Aparecida [UNIFESP] Bonetti, Tatiana Carvalho de Souza [UNIFESP] Albertoni, Guilherme Ambrozio [UNIFESP] Schor, Eduardo [UNIFESP] Barreto, Jose A. Oliva, Maria Luiza Vilela [UNIFESP] Juliano, Luiz [UNIFESP] Girão, Manoel João Batista Castello [UNIFESP] Silva, Ismael Dale Cotrim Guerreiro da [UNIFESP] |
author2_role |
author author author author author author author author author author author author |
dc.contributor.institution.none.fl_str_mv |
Universidade Federal de São Paulo (UNIFESP) Charitable Assoc Blood Collect |
dc.contributor.author.fl_str_mv |
Andrade, Sheila Siqueira [UNIFESP] Azevedo, Aline de Cássia [UNIFESP] Monasterio, Izabel C. G. [UNIFESP] Paredes-Gamero, Edgar Julian [UNIFESP] Gonçalves, Giovana Aparecida [UNIFESP] Bonetti, Tatiana Carvalho de Souza [UNIFESP] Albertoni, Guilherme Ambrozio [UNIFESP] Schor, Eduardo [UNIFESP] Barreto, Jose A. Oliva, Maria Luiza Vilela [UNIFESP] Juliano, Luiz [UNIFESP] Girão, Manoel João Batista Castello [UNIFESP] Silva, Ismael Dale Cotrim Guerreiro da [UNIFESP] |
dc.subject.eng.fl_str_mv |
Endometriosis 17 beta-Estradiol Hydrogen peroxide Free radicals |
topic |
Endometriosis 17 beta-Estradiol Hydrogen peroxide Free radicals |
description |
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. |
publishDate |
2013 |
dc.date.issued.fl_str_mv |
2013-07-01 |
dc.date.accessioned.fl_str_mv |
2016-01-24T14:31:54Z |
dc.date.available.fl_str_mv |
2016-01-24T14:31:54Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.citation.fl_str_mv |
Free Radical Biology and Medicine. New York: Elsevier B.V., v. 60, p. 63-72, 2013. |
dc.identifier.uri.fl_str_mv |
http://repositorio.unifesp.br/handle/11600/36441 http://dx.doi.org/10.1016/j.freeradbiomed.2013.01.034 |
dc.identifier.issn.none.fl_str_mv |
0891-5849 |
dc.identifier.file.none.fl_str_mv |
WOS000319486500009.pdf |
dc.identifier.doi.none.fl_str_mv |
10.1016/j.freeradbiomed.2013.01.034 |
dc.identifier.wos.none.fl_str_mv |
WOS:000319486500009 |
identifier_str_mv |
Free Radical Biology and Medicine. New York: Elsevier B.V., v. 60, p. 63-72, 2013. 0891-5849 WOS000319486500009.pdf 10.1016/j.freeradbiomed.2013.01.034 WOS:000319486500009 |
url |
http://repositorio.unifesp.br/handle/11600/36441 http://dx.doi.org/10.1016/j.freeradbiomed.2013.01.034 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.ispartof.none.fl_str_mv |
Free Radical Biology and Medicine |
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http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy info:eu-repo/semantics/openAccess |
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http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy |
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openAccess |
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63-72 |
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Elsevier B.V. |
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Elsevier B.V. |
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