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

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

Author Andrade, Sheila Siqueira Autor UNIFESP Google Scholar
Azevedo, Aline de Cássia Autor UNIFESP Google Scholar
Monasterio, Izabel C. G. Autor UNIFESP Google Scholar
Paredes-Gamero, Edgar Julian Autor UNIFESP Google Scholar
Gonçalves, Giovana Aparecida Autor UNIFESP Google Scholar
Bonetti, Tatiana Carvalho de Souza Autor UNIFESP Google Scholar
Albertoni, Guilherme Ambrozio Autor UNIFESP Google Scholar
Schor, Eduardo Autor UNIFESP Google Scholar
Barreto, Jose A. Google Scholar
Oliva, Maria Luiza Vilela Autor UNIFESP Google Scholar
Juliano, Luiz Autor UNIFESP Google Scholar
Girão, Manoel João Batista Castello Autor UNIFESP Google Scholar
Silva, Ismael Dale Cotrim Guerreiro da Autor UNIFESP Google Scholar
Institution Universidade Federal de São Paulo (UNIFESP)
Charitable Assoc Blood Collect
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.
Keywords Endometriosis
17 beta-Estradiol
Hydrogen peroxide
Free radicals
Language English
Sponsor Associacao Beneficente de Coleta de Sangue
Fundação 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)
Date 2013-07-01
Published in Free Radical Biology and Medicine. New York: Elsevier B.V., v. 60, p. 63-72, 2013.
ISSN 0891-5849 (Sherpa/Romeo, impact factor)
Publisher Elsevier B.V.
Extent 63-72
Origin http://dx.doi.org/10.1016/j.freeradbiomed.2013.01.034
Access rights Open access Open Access
Type Article
Web of Science ID WOS:000319486500009
URI http://repositorio.unifesp.br/handle/11600/36441

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