Navegando por Palavras-chave "17 beta-Estradiol"

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    17 beta-Estradiol and steady-state concentrations of H2O2: antiapoptotic effect in endometrial cells from patients with endometriosis
    (Elsevier B.V., 2013-07-01) 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 Collect
    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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    Estrogen receptor ESR1 regulates the phospholipase C-inositol phosphate signaling in the hippocampus from rats in proestrous and estrous phases
    (Elsevier B.V., 2013-01-01) Maruyama, Nadia O.; Lucas, Thais F. G. [UNIFESP]; Porto, Catarina S. [UNIFESP]; Abdalla, Fernando M. F.; Inst Butantan; Universidade Federal de São Paulo (UNIFESP)
    The aim of the present study was to investigate the involvement of estrogen receptors in the activation of phospholipase C (PLC)-phosphoinositide hydrolysis in the hippocampus from rats in estrous and proestrous phases. 17 beta-Estradiol (E2) and ESR1 -selective agonist PPT, but not ESR2-selective agonist DPN, induced a rapid increase on total [H-3]-inositol phosphate accumulation in the hippocampus from both rats. These effects are mediated by PLC activation, since the inhibition of this protein decreased the total [H-3]-inositol phosphate accumulation. the pretreatment with ESR1 and ESR2 antagonist ICI 182,780, but not with GPER antagonist G-15, blocked the total [H-3]-inositol phosphate accumulation induced by E2 and PPT, confirming that ESR1 is upstream component regulating this rapid effect. SRC family of protein tyrosine kinases inhibitor PP2 blocked the total [H-3]-inositol phosphate accumulation induced by E2 and PPT in hippocampus, suggesting that ESR1 undergoes translocation from the nuclei to the plasma membrane region via SRC to activate rapid signaling pathways. Furthermore, the magnitude of the response to E2 and PPT was higher in hippocampus from rats in proestrous than in estrous. On the other hand, the expression of the ESR1 is higher in hippocampus from rats in estrous than in proestrous, indicating that the regulation of this receptor by estrous cycle does not play a role in the magnitude of the response to E2 and PPT in hippocampus. in conclusion, our results indicate that E2 activates SRC-mediated translocation of ESR1 to the plasma membrane, which results in the activation of PLC-inositol phosphate signaling pathway in rat hippocampus. Thus, these rapid estrogen actions in hippocampus might be a key step mediating cellular events important for learning and memory. (C) 2012 Elsevier Inc. All rights reserved.
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    Estrogen receptors mediate rapid activation of phospholipase C pathway in the rat endometrium
    (Elsevier B.V., 2011-12-20) Konigame, Vivian Cristina; Siu, Erica Rosanna [UNIFESP]; Royer, Carine [UNIFESP]; Lucas, Thais Fabiana Gameiro [UNIFESP]; Porto, Catarina Segreti [UNIFESP]; Abdalla, Fernando Mauricio Francis; Inst Butantan; Universidade Federal de São Paulo (UNIFESP)
    The 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.
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    Ovariectomy and 17 beta-estradiol replacement play a role on the expression of Endonuclease-G and phosphorylated cyclic AMP response element-binding (CREB) protein in hippocampus
    (Elsevier B.V., 2014-01-25) Santos Pereira, Renato Tavares dos; Porto, Catarina Segreti [UNIFESP]; Francis Abdalla, Fernando Mauricio; Inst Butantan; Universidade Federal de São Paulo (UNIFESP)
    The aim of the present study was to investigate the effects of different periods of ovariectomy and 17 beta-estradiol (E2) replacement on the expression of Cytochrome C, apoptosis inducing factor (AIF) and Endonuclease-G (Endo-G) in mitochondrial and cytosolic fractions obtained from hippocampus of the adult female rats. in addition, the expression of phosphorylated CREB (phospho-CREB) was also analyzed in hippocampus. Ovariectomy or E2 treatment did not change the expression of Cytochrome C and AIF. Ovariectomy (15, 21 and 36 days) decreased the expression of Endo-G in the mitochondrial fractions and increased it in the cytosolic fractions obtained from hippocampus. the treatment with E2 after 15 days of ovariectomy for 7 days or 21 days, and throughout the post-ovariectomy period prevented the effects of ovariectomy on Endo-G expression. Our results suggest that ovariectomy-induced apoptotic cell death in hippocampal tissue could be mediated by Endo-G, but not by AIF, via a caspase-independent apoptotic pathway. Furthermore, ovariectomy decreased the expression of phospho-CREB and the treatment with E2 prevented these effects. in conclusion, E2 may help maintain long-term neuronal viability by regulating the expression of members of the Bcl-2 family. Regulation of Endo-G released from mitochondria, but not of Cytochrome C and AIF, is also involved in the neuroprotective actions of E2. Furthermore, CREB may be involved in the expression of Bcl-2. These data provide new understanding into the mechanisms involved in the neuroprotective role of estrogen. (C) 2013 Elsevier Ireland Ltd. All rights reserved.