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17alpha Estradiol

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Erika Navarrete – One of the best experts on this subject based on the ideXlab platform.

  • Evidence that 17alphaEstradiol is biologically active in the uterine tissue: Antiuterotonic and antiuterotrophic action
    Reproductive Biology and Endocrinology, 2005
    Co-Authors: Mercedes Perusquía, Erika Navarrete

    Abstract:

    Background 17alphaEstradiol has been considered as the hormonally inactive isomer of 17beta-Estradiol. Recently, nongenomic (smooth muscle relaxation) and genomic (light estrogenic activity) effects of 17alphaEstradiol have been reported, but no reports have yet determined its possible antiestrogenic activity. Therefore, this study investigated: the nongenomic action of 17alphaEstradiol on uterine contractile activity and its potential agonist-antagonist activity on uterine growth. Methods Uterine rings from rats were isometrically recorded. Different concentrations (0.2–200 microM) of 17alphaEstradiol were tested on spontaneous contraction and equimolarly compared with 17beta-Estradiol. To examine the mechanism of 17alphaEstradiol action, its effect was studied in presence of beta2-antagonist (propranolol), antiestrogens (tamoxifen and ICI 182,780) or inhibitors of protein synthesis (cycloheximide) and transcription (actinomycin D). Moreover, contractions induced by high potassium (KCl) solution or calcium in depolarized tissues by KCl-calcium free solution were exposed to 17alphaEstradiol. Collaterally, we performed an uterotrophic assay in adult ovariectomized rats measuring the uterine wet weight. The administration for three days of 0.3 microM/day/Kg 17beta-Estradiol was equimolarly compared with the response produced by 17alphaEstradiol. Antiuterotrophic activity was assayed by administration of 0.3 microM/day/Kg 17beta-Estradiol and various doses ratios (1:1, 1:3, 1:5, and 1:100) of 17alphaEstradiol. Results The Estradiol isomers elicited an immediate relaxation, concentration-dependent and reversible on spontaneous contraction. 17alphaEstradiol presented lower potency than 17beta-Estradiol although it did not antagonize 17beta-Estradiol-induced relaxation. Relaxation to 17alphaEstradiol was not inhibited by propranolol, tamoxifen, ICI 182,780, cycloheximide or actinomycin D. The KCl contractions were also sensitive to 17alphaEstradiol-induced relaxation and calcium contractions in depolarized tissues were markedly prevented by 17alphaEstradiol, implying a reduction of extracellular calcium influx through voltage-operated calcium channels (VOCCs). Uterotrophic assay detected significant increase in uterine weight using 17alphaEstradiol, which was significantly minor as compared with 17beta-Estradiol. 17alphaEstradiol, at all doses ratios, significantly antagonized the hypertrophic response of 17beta-Estradiol. Conclusion 17alphaEstradiol induces a relaxing effect, which may be independent of the classical estrogen receptor, nongenomic action, apparently mediated by inactivation of VOCCs. 17alphaEstradiol is also a weak estrogen agonist (uterotrophic response); likewise, 17alphaEstradiol may act as an antiestrogen (antiuterotrophic response). The overall data document a nongenomic relaxing action and a novel antiestrogenic action of 17alphaEstradiol, which are relevant in estrogen-mediated uterine physiology.

  • evidence that 17alpha Estradiol is biologically active in the uterine tissue antiuterotonic and antiuterotrophic action
    Reproductive Biology and Endocrinology, 2005
    Co-Authors: Mercedes Perusquía, Erika Navarrete

    Abstract:

    Background
    17alphaEstradiol has been considered as the hormonally inactive isomer of 17beta-Estradiol. Recently, nongenomic (smooth muscle relaxation) and genomic (light estrogenic activity) effects of 17alphaEstradiol have been reported, but no reports have yet determined its possible antiestrogenic activity. Therefore, this study investigated: the nongenomic action of 17alphaEstradiol on uterine contractile activity and its potential agonist-antagonist activity on uterine growth.

  • Evidence that 17alphaEstradiol is biologically active in the uterine tissue: antiuterotonic and antiuterotrophic action.
    Reproductive biology and endocrinology : RB&E, 2005
    Co-Authors: Mercedes Perusquía, Erika Navarrete

    Abstract:

    Background: 17alphaEstradiol has been considered as the hormonally inactive isomer of 17beta-Estradiol. Recently, nongenomic (smooth muscle relaxation) and genomic (light estrogenic activity) effects of 17alphaEstradiol have been reported, but no reports have yet determined its possible antiestrogenic activity. Therefore, this study investigated: the nongenomic action of 17alphaEstradiol on uterine contractile activity and its potential agonist-antagonist activity on uterine growth. Methods: Uterine rings from rats were isometrically recorded. Different concentrations (0.2–200 microM) of 17alphaEstradiol were tested on spontaneous contraction and equimolarly compared with 17beta-Estradiol. To examine the mechanism of 17alphaEstradiol action, its effect was studied in presence of beta2-antagonist (propranolol), antiestrogens (tamoxifen and ICI 182,780) or inhibitors of protein synthesis (cycloheximide) and transcription (actinomycin D). Moreover, contractions induced by high potassium (KCl) solution or calcium in depolarized tissues by KCl-calcium free solution were exposed to 17alphaEstradiol. Collaterally, we performed an uterotrophic assay in adult ovariectomized rats measuring the uterine wet weight. The administration for three days of 0.3 microM/day/Kg 17beta-Estradiol was equimolarly compared with the response produced by 17alphaEstradiol. Antiuterotrophic activity was assayed by administration of 0.3 microM/day/Kg 17beta-Estradiol and various doses ratios (1:1, 1:3, 1:5, and 1:100) of 17alphaEstradiol.

Akihisa Iguchi – One of the best experts on this subject based on the ideXlab platform.

  • 17beta-Estradiol inhibits NADPH oxidase activity through the regulation of p47phox mRNA and protein expression in THP-1 cells.
    Biochimica et biophysica acta, 2003
    Co-Authors: Daigo Sumi, Toshio Hayashi, Hisako Matsui-hirai, Aaron T. Jacobs, Louis J. Ignarro, Akihisa Iguchi

    Abstract:

    In this report, we demonstrate that NADPH oxidase is activated by tumor necrosis factor-alpha (TNF-alpha) plus interferon-gamma (IFN-gamma) in human monocytic cells (THP-1 cells) differentiated with phorbol ester (PMA) and that physiological concentration of 17beta-Estradiol inhibits NADPH oxidase activity in THP-1 cells stimulated with TNF-alpha plus IFN-gamma. This effect is mediated by estrogen receptor based on estrogen receptor antagonist (ICI 182, 780) that diminishes inhibition by 17beta-Estradiol. This inhibition is specific in 17beta-Estradiol because 17alphaEstradiol, testosterone and progesterone do not inhibit NADPH oxidase activity. Activation of NADPH oxidase induced by TNF-alpha plus IFN-gamma is caused by up-regulation of p47(phox) (cytosolic component of NADPH oxidase) expression. 17beta-Estradiol prevents the up-regulation of p47(phox) mRNA and protein expression. This prevention of p47(phox) expression depends on the inhibition of NF-kappaB activation. Our results implicate that 17beta-Estradiol has an anti-atherosclerotic effects through the improvement of nitric oxide (NO) bioavailability caused by the regulation of superoxide (O(2)(-)) production.

  • 17β-Estradiol inhibits NADPH oxidase activity through the regulation of p47phox mRNA and protein expression in THP-1 cells
    Biochimica et Biophysica Acta, 2003
    Co-Authors: Daigo Sumi, Toshio Hayashi, Hisako Matsui-hirai, Aaron T. Jacobs, Louis J. Ignarro, Akihisa Iguchi

    Abstract:

    In this report, we demonstrate that NADPH oxidase is activated by tumor necrosis factor-alpha (TNF-alpha) plus interferon-gamma (IFN-gamma) in human monocytic cells (THP-1 cells) differentiated with phorbol ester (PMA) and that physiological concentration of 17beta-Estradiol inhibits NADPH oxidase activity in THP-1 cells stimulated with TNF-alpha plus IFN-gamma. This effect is mediated by estrogen receptor based on estrogen receptor antagonist (ICI 182, 780) that diminishes inhibition by 17beta-Estradiol. This inhibition is specific in 17beta-Estradiol because 17alphaEstradiol, testosterone and progesterone do not inhibit NADPH oxidase activity. Activation of NADPH oxidase induced by TNF-alpha plus IFN-gamma is caused by up-regulation of p47(phox) (cytosolic component of NADPH oxidase) expression. 17beta-Estradiol prevents the up-regulation of p47(phox) mRNA and protein expression. This prevention of p47(phox) expression depends on the inhibition of NF-kappaB activation. Our results implicate that 17beta-Estradiol has an anti-atherosclerotic effects through the improvement of nitric oxide (NO) bioavailability caused by the regulation of superoxide (O(2)(-)) production.

  • Physiological concentrations of 17β-Estradiol inhibit the synthesis of nitric oxide synthase in macrophages via a receptor-mediated system
    Journal of cardiovascular pharmacology, 1998
    Co-Authors: Toshio Hayashi, Kazuyoshi Yamada, Teiji Esaki, Emiko Muto, Gautam Chaudhuri, Akihisa Iguchi

    Abstract:

    We investigated the effect of estrogen on inducible nitric oxide synthase (iNOS), which is not well understood, in contrast to the known effect of estrogen on endothelial nitric oxide synthase (eNOS). When J774 cells, a murine macrophage cell line, were incubated with interferon-gamma and lipopolysaccharide, iNOS was induced, and a large amount of NO was released. Pre- or coincubation with 17beta-Estradiol inhibited this induction of iNOS protein and NO release; however, 17beta-Estradiol did not have a direct effect on enzyme activity of iNOS. The analog, 17alphaEstradiol, did not have such an effect. Tamoxifen, an antiestrogen, and ICI182780, an estrogen-receptor antagonist, inhibited the influence of 17beta-Estradiol on iNOS. Thus 17beta-Estradiol inhibited the induction of iNOS by a classic receptor-mediated pathway. The inhibition of the NO release from iNOS by 17beta-Estradiol is in contrast to the reported augmentation of continuous NO release from eNOS. These harmonious effects of estrogen on iNOS and eNOS may have some role in the antiatherosclerotic effects of 17beta-Estradiol.

Mercedes Perusquía – One of the best experts on this subject based on the ideXlab platform.

  • Evidence that 17alphaEstradiol is biologically active in the uterine tissue: Antiuterotonic and antiuterotrophic action
    Reproductive Biology and Endocrinology, 2005
    Co-Authors: Mercedes Perusquía, Erika Navarrete

    Abstract:

    Background 17alphaEstradiol has been considered as the hormonally inactive isomer of 17beta-Estradiol. Recently, nongenomic (smooth muscle relaxation) and genomic (light estrogenic activity) effects of 17alphaEstradiol have been reported, but no reports have yet determined its possible antiestrogenic activity. Therefore, this study investigated: the nongenomic action of 17alphaEstradiol on uterine contractile activity and its potential agonist-antagonist activity on uterine growth. Methods Uterine rings from rats were isometrically recorded. Different concentrations (0.2–200 microM) of 17alphaEstradiol were tested on spontaneous contraction and equimolarly compared with 17beta-Estradiol. To examine the mechanism of 17alphaEstradiol action, its effect was studied in presence of beta2-antagonist (propranolol), antiestrogens (tamoxifen and ICI 182,780) or inhibitors of protein synthesis (cycloheximide) and transcription (actinomycin D). Moreover, contractions induced by high potassium (KCl) solution or calcium in depolarized tissues by KCl-calcium free solution were exposed to 17alphaEstradiol. Collaterally, we performed an uterotrophic assay in adult ovariectomized rats measuring the uterine wet weight. The administration for three days of 0.3 microM/day/Kg 17beta-Estradiol was equimolarly compared with the response produced by 17alphaEstradiol. Antiuterotrophic activity was assayed by administration of 0.3 microM/day/Kg 17beta-Estradiol and various doses ratios (1:1, 1:3, 1:5, and 1:100) of 17alphaEstradiol. Results The Estradiol isomers elicited an immediate relaxation, concentration-dependent and reversible on spontaneous contraction. 17alphaEstradiol presented lower potency than 17beta-Estradiol although it did not antagonize 17beta-Estradiol-induced relaxation. Relaxation to 17alphaEstradiol was not inhibited by propranolol, tamoxifen, ICI 182,780, cycloheximide or actinomycin D. The KCl contractions were also sensitive to 17alphaEstradiol-induced relaxation and calcium contractions in depolarized tissues were markedly prevented by 17alphaEstradiol, implying a reduction of extracellular calcium influx through voltage-operated calcium channels (VOCCs). Uterotrophic assay detected significant increase in uterine weight using 17alphaEstradiol, which was significantly minor as compared with 17beta-Estradiol. 17alphaEstradiol, at all doses ratios, significantly antagonized the hypertrophic response of 17beta-Estradiol. Conclusion 17alphaEstradiol induces a relaxing effect, which may be independent of the classical estrogen receptor, nongenomic action, apparently mediated by inactivation of VOCCs. 17alphaEstradiol is also a weak estrogen agonist (uterotrophic response); likewise, 17alphaEstradiol may act as an antiestrogen (antiuterotrophic response). The overall data document a nongenomic relaxing action and a novel antiestrogenic action of 17alphaEstradiol, which are relevant in estrogen-mediated uterine physiology.

  • evidence that 17alpha Estradiol is biologically active in the uterine tissue antiuterotonic and antiuterotrophic action
    Reproductive Biology and Endocrinology, 2005
    Co-Authors: Mercedes Perusquía, Erika Navarrete

    Abstract:

    Background
    17alphaEstradiol has been considered as the hormonally inactive isomer of 17beta-Estradiol. Recently, nongenomic (smooth muscle relaxation) and genomic (light estrogenic activity) effects of 17alphaEstradiol have been reported, but no reports have yet determined its possible antiestrogenic activity. Therefore, this study investigated: the nongenomic action of 17alphaEstradiol on uterine contractile activity and its potential agonist-antagonist activity on uterine growth.

  • Evidence that 17alphaEstradiol is biologically active in the uterine tissue: antiuterotonic and antiuterotrophic action.
    Reproductive biology and endocrinology : RB&E, 2005
    Co-Authors: Mercedes Perusquía, Erika Navarrete

    Abstract:

    Background: 17alphaEstradiol has been considered as the hormonally inactive isomer of 17beta-Estradiol. Recently, nongenomic (smooth muscle relaxation) and genomic (light estrogenic activity) effects of 17alphaEstradiol have been reported, but no reports have yet determined its possible antiestrogenic activity. Therefore, this study investigated: the nongenomic action of 17alphaEstradiol on uterine contractile activity and its potential agonist-antagonist activity on uterine growth. Methods: Uterine rings from rats were isometrically recorded. Different concentrations (0.2–200 microM) of 17alphaEstradiol were tested on spontaneous contraction and equimolarly compared with 17beta-Estradiol. To examine the mechanism of 17alphaEstradiol action, its effect was studied in presence of beta2-antagonist (propranolol), antiestrogens (tamoxifen and ICI 182,780) or inhibitors of protein synthesis (cycloheximide) and transcription (actinomycin D). Moreover, contractions induced by high potassium (KCl) solution or calcium in depolarized tissues by KCl-calcium free solution were exposed to 17alphaEstradiol. Collaterally, we performed an uterotrophic assay in adult ovariectomized rats measuring the uterine wet weight. The administration for three days of 0.3 microM/day/Kg 17beta-Estradiol was equimolarly compared with the response produced by 17alphaEstradiol. Antiuterotrophic activity was assayed by administration of 0.3 microM/day/Kg 17beta-Estradiol and various doses ratios (1:1, 1:3, 1:5, and 1:100) of 17alphaEstradiol.