17 beta-Estradiol and steady-state concentrations of H2O2: antiapoptotic effect in endometrial cells from patients with endometriosis
Data
2013-07-01
Autores
Andrade, Sheila Siqueira 
Azevedo, Aline de Cássia
Monasterio, Izabel C. G.
Paredes-Gamero, Edgar Julian
Gonçalves, Giovana Aparecida
Mostrar mais
Tipo
Artigo
Título da Revista
ISSN da Revista
Título de Volume
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.
Descrição
Citação
Free Radical Biology and Medicine. New York: Elsevier B.V., v. 60, p. 63-72, 2013.