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Готові списки джерел за темами / Estrogen (17β estradiol) / Статті в журналах

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Статті в журналах з теми "Estrogen (17β estradiol)"

Автор: Grafiati

Опубліковано: 3 червня 2025

Оновлено: 31 липня 2025

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1

Ansell, P. J., C. Espinosa-Nicholas, E. M. Curran, et al. "In Vitro and in Vivo Regulation of Antioxidant Response Element-Dependent Gene Expression by Estrogens." Endocrinology 145, no. 1 (2004): 311–17. http://dx.doi.org/10.1210/en.2003-0817.

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Abstract Understanding estrogen’s regulation of phase II detoxification enzymes is important in explaining how estrogen exposure increases the risk of developing certain cancers. Phase II enzymes such as glutathione-S-transferases (GST) and quinone reductase protect against developing chemically induced cancers by metabolizing reactive oxygen species. Phase II enzyme expression is regulated by a cis-acting DNA sequence, the antioxidant response element (ARE). It has previously been reported that several antiestrogens, but not 17β-estradiol, could regulate ARE-mediated gene transcription. Our g

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2

Jayachandran, Muthuvel, Antonio Sanzo, Whyte G. Owen, and Virginia M. Miller. "Estrogenic regulation of tissue factor and tissue factor pathway inhibitor in platelets." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 5 (2005): H1908—H1916. http://dx.doi.org/10.1152/ajpheart.01292.2004.

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Oral estrogen treatment increases thrombotic risk. Tissue factor (TF), tissue factor pathway inhibitor (TFPI), and platelet interaction with leukocytes are important determinants of thrombogenesis. Therefore, the present study was designed to define and compare platelet TF and TFPI mRNA and adhesion protein expression in platelets derived from animals treated with different types of oral estrogens. Ovariectomized pigs were treated with 17β-estradiol (2 mg/day), conjugated equine estrogen (CEE; 0.625 mg/day), or raloxifene (60 mg/day) for 4 wk. Compared with intact animals, ovariectomy and trea

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3

Moro, Laura, Stefania Reineri, Daniela Piranda та ін. "Nongenomic effects of 17β-estradiol in human platelets: potentiation of thrombin-induced aggregation through estrogen receptor β and Src kinase". Blood 105, № 1 (2005): 115–21. http://dx.doi.org/10.1182/blood-2003-11-3840.

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Abstract The impact of estrogens on the cardiovascular system and their ability to regulate platelet function are matters of controversy. The recent finding that estrogen receptors are expressed in human platelets renders these cells an excellent model for studying the nongenomic effects of these hormones. In this work, we investigated 17β-estradiol–dependent signaling in platelets from adult healthy men. 17β-estradiol caused the rapid phosphorylation of the tyrosine kinases Src and Pyk2 and the formation of a signaling complex, which included Src, Pyk2, and the phosphatidylinositol 3-kinase.

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4

Hillerns, Pablo Ibieta, Yuangang Zu, and Michael Wink. "Binding of Phytoestrogens to Rat Uterine Estrogen Receptors and Human Sex Hormone-binding Globulins." Zeitschrift für Naturforschung C 60, no. 7-8 (2005): 649–56. http://dx.doi.org/10.1515/znc-2005-7-823.

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The interaction of phytoestrogens with the most important binding sites of steroid hormones, i.e. sex hormone-binding globulin and estrogen receptors, was investigated. Relative binding affinities and association constants for 21 compounds among them isoflavones, flavones, flavonols, flavanones, chalcones and lignans were determined. The lignan nordihydroguaiaretic acid weakly displaced 17β-[3H]-estradiol from estrogen receptor and Scatchard analysis suggests non-conformational changes. Compounds from Glycyrrhiza glabra, liquiritigenin and isoliquiritigenin, showed estrogenic affinities to bot

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5

Kennedy, Angela M., Kristen L. Shogren, Minzhi Zhang, Russell T. Turner, Thomas C. Spelsberg та Avudaiappan Maran. "17β-Estradiol-Dependent Activation of Signal Transducer and Activator of Transcription-1 in Human Fetal Osteoblasts Is Dependent on Src Kinase Activity". Endocrinology 146, № 1 (2005): 201–7. http://dx.doi.org/10.1210/en.2004-0486.

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Estrogen is essential for normal growth and remodeling of bone. Although the mechanism of estrogen action on bone cells has been widely investigated, the full spectrum of signal transduction pathways activated by estrogen is unknown. In this report, we investigate the effects of the gonadal hormone 17β-estradiol on the regulation of signal transducer and activator of transcription-1 (Stat1) protein in cultured human fetal osteoblast cells, devoid of the classical estrogen receptors (ERs). 17β-Estradiol (10 nm) led to rapid (within 15 min) activation of Stat1 protein as indicated by increases i

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6

Culmsee, Carsten, Helmut Vedder, Alexander Ravati, et al. "Neuroprotection by Estrogens in a Mouse Model of Focal Cerebral Ischemia and in Cultured Neurons: Evidence for a Receptor-Independent Antioxidative Mechanism." Journal of Cerebral Blood Flow & Metabolism 19, no. 11 (1999): 1263–69. http://dx.doi.org/10.1097/00004647-199911000-00011.

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Estrogens have been suggested for the treatment of neurodegenerative disorders, including stroke, because of their neuroprotective activities against various neurotoxic stimuli such as glutamate, glucose deprivation, iron, or β-amyloid. Here, the authors report that 17β-estradiol (0.3 to 30 mg/kg) and 2-OH-estradiol (0.003 to 30 mg/kg) reduced brain tissue damage after permanent occlusion of the middle cerebral artery in male NMRI mice. In vitro, 17β-estradiol (1 to 10 μmol/L) and 2-OH-estradiol (0.01 to 1 μmol/L) reduced the percentage of damaged chick embryonic neurons treated with FeSO4. In

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7

Kaun, Christoph, Gersina Rega, Walter Speidl та ін. "The estrogen metabolite 17β-dihydroequilenin counteracts interleukin-1α induced expression of inflammatory mediators in human endothelial cells in vitro via NF-κB pathway". Thrombosis and Haemostasis 95, № 01 (2006): 107–16. http://dx.doi.org/10.1160/th05-05-0333.

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SummaryIn most studies showing cardio- and vasculoprotective effects of estrogens, 17β-estradiol was used and little information on possible effects of different estrogen metabolites is yet available. We investigated whether particular estrogen metabolites are effective in counteracting inflammatory activation of human endothelium. Human endothelial cells were incubated with 17α-dihydroequilenin, 17β-dihydroequilenin, δ-8,9-dehydroestrone, estrone and 17β-estradiol and stimulated with interleukin (IL)-1α.The expression of IL-6, IL-8 and monocyte chemoattractant protein-1 (MCP-1) was determined

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8

Cho, JungYoon, Wankyu Park, SeungKi Lee, Woongshick Ahn та YoungJoo Lee. "Ginsenoside-Rb1 from Panax ginseng C.A. Meyer Activates Estrogen Receptor-α and -β, Independent of Ligand Binding". Journal of Clinical Endocrinology & Metabolism 89, № 7 (2004): 3510–15. http://dx.doi.org/10.1210/jc.2003-031823.

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Abstract We studied the estrogenic activity of a component of Panax ginseng, ginsenoside-Rb1. The activity of ginsenoside-Rb1 was characterized in a transient transfection system, using estrogen receptor isoforms and estrogen-responsive luciferase plasmids, in COS monkey kidney cells. Ginsenoside-Rb1 activated both α and β estrogen receptors in a dose-dependent manner with maximal activity observed at 100 μm, the highest concentration examined. Activation was inhibited by the estrogen receptor antagonist ICI 182,780, indicating that the effects were mediated through the estrogen receptor. Trea

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9

Rodríguez-Landa, Juan Francisco, Oscar Jerónimo Olmos-Vázquez, Carlos Fabrizio Quiñonez-Bailón, et al. "Genistein Reduces Anxiety-like Behavior During Metestrus–Diestrus Phase Without Changing Estradiol or Progesterone Levels in Wistar Rats." Metabolites 15, no. 5 (2025): 311. https://doi.org/10.3390/metabo15050311.

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Background: Premenstrual syndrome is characterized by emotional changes, including anxiety and depression symptoms, which may be treated with anxiolytic and antidepressant drugs, as well as estrogen therapy. However, steroidal estrogen therapy is contraindicated for patients with a potential risk of developing estrogen-dependent cancers through interactions with estrogen receptor α (ERα). Alternatively, genistein produces estrogenic effects in animals and humans at dietary dosages that act on the nuclear and membrane ERα, estrogen receptor β (ERβ), and the G-protein-coupled estrogen receptor (

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10

Jayachandran, Muthuvel, Rajarshi Mukherjee, Thomas Steinkamp та ін. "Differential effects of 17β-estradiol, conjugated equine estrogen, and raloxifene on mRNA expression, aggregation, and secretion in platelets". American Journal of Physiology-Heart and Circulatory Physiology 288, № 5 (2005): H2355—H2362. http://dx.doi.org/10.1152/ajpheart.01108.2004.

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Changes in platelet functions could contribute to thrombotic risk associated with estrogen treatments. This study was designed to test the hypothesis that three clinically relevant estrogenic treatments affect platelet function comparably. Adult female pigs were ovariectomized and randomized to either no treatment or treatment with oral 17β-estradiol (2 mg/day), conjugated equine estrogen (0.625 mg/day), or raloxifene (60 mg/day) for 4 wk. Platelet turnover, aggregation, and secretion were assessed before and after treatment. Platelet turnover and mRNA increased significantly only in pigs trea

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11

Pentikäinen, Virve, Krista Erkkilä, Laura Suomalainen, Martti Parvinen, and Leo Dunkel. "Estradiol Acts as a Germ Cell Survival Factor in the Human Testis in Vitro*." Journal of Clinical Endocrinology & Metabolism 85, no. 5 (2000): 2057–67. http://dx.doi.org/10.1210/jcem.85.5.6600.

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Abstract The necessity of estrogens for male fertility was recently discovered in studies on both estrogen receptor α knockout and aromatase (cyp 19 gene) knockout mice. However, direct testicular effects of estrogens in male reproduction have remained unclear. Here we studied the protein expression of ERα and the recently described estrogen receptor β in the human seminiferous epithelium and evaluated the role of 17β-estradiol, the main physiological estrogen, in male germ cell survival. Interestingly, both estrogen receptors α and β were found in early meiotic spermatocytes and elongating sp

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12

Stefano, George B., Vincent Prevot, Jean-Claude Beauvillain, et al. "Estradiol Coupling to Human Monocyte Nitric Oxide Release Is Dependent on Intracellular Calcium Transients: Evidence for an Estrogen Surface Receptor." Journal of Immunology 163, no. 7 (1999): 3758–63. http://dx.doi.org/10.4049/jimmunol.163.7.3758.

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Abstract We tested the hypothesis that estrogen acutely stimulates constitutive NO synthase (cNOS) activity in human peripheral monocytes by acting on an estrogen surface receptor. NO release was measured in real time with an amperometric probe. 17β-estradiol exposure to monocytes stimulated NO release within seconds in a concentration-dependent manner, whereas 17α-estradiol had no effect. 17β-estradiol conjugated to BSA (E2-BSA) also stimulated NO release, suggesting mediation by a membrane surface receptor. Tamoxifen, an estrogen receptor inhibitor, antagonized the action of both 17β-estradi

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13

Napolitano, Mariarosaria, Ida Blotta, Anna Montali та Elena Bravo. "17β-Estradiol Enhances the Flux of Cholesterol Through the Cholesteryl Ester Cycle in Human Macrophages". Bioscience Reports 21, № 5 (2001): 637–52. http://dx.doi.org/10.1023/a:1014721026280.

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Estrogens have been shown to have many positive effects on the function of arterial wall, and recent evidence suggest that 17β-estradiol has a direct action in reducing the accumulation of cholesteryl ester in macrophages. The mechanisms underlying the effects of 17β-estradiol on foam cell formation, however are poorly understood. The aim of this study is to investigate the role of 17β-estradiol in the regulation of the cholesteryl ester cycle and cholesterol efflux in human macrophages. In addition, the influence of 17β-estradiol on apolipoprotein E (apoE) and lipoprotein lipase (LDL) secreti

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14

Bühler, Miriam, Jeanine Fahrländer, Alexander Sauter, et al. "GPER1 links estrogens to centrosome amplification and chromosomal instability in human colon cells." Life Science Alliance 6, no. 1 (2022): e202201499. http://dx.doi.org/10.26508/lsa.202201499.

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The role of the alternate G protein–coupled estrogen receptor 1 (GPER1) in colorectal cancer (CRC) development and progression is unclear, not least because of conflicting clinical and experimental evidence for pro- and anti-tumorigenic activities. Here, we show that low concentrations of the estrogenic GPER1 ligands, 17β-estradiol, bisphenol A, and diethylstilbestrol cause the generation of lagging chromosomes in normal colon and CRC cell lines, which manifest in whole chromosomal instability and aneuploidy. Mechanistically, (xeno)estrogens triggered centrosome amplification by inducing centr

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15

Hutchens, Michael P., Tetsuhiro Fujiyoshi, Radko Komers, Paco S. Herson, and Sharon Anderson. "Estrogen protects renal endothelial barrier function from ischemia-reperfusion in vitro and in vivo." American Journal of Physiology-Renal Physiology 303, no. 3 (2012): F377—F385. http://dx.doi.org/10.1152/ajprenal.00354.2011.

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Emerging evidence suggests that renal endothelial function may be altered in ischemia-reperfusion injury. Acute kidney injury is sexually dimorphic, and estrogen protects renal tubular function after experimental ischemic injury. This study tested the hypothesis that during ischemia-reperfusion, estrogen alters glomerular endothelial function to prevent hyperpermeability. Glomerular endothelial cells were exposed to 8-h oxygen-glucose deprivation (OGD) followed by 4- and 8-h reoxygenation-glucose repletion. After 4-h reoxygenation-glucose repletion, transendothelial permeability to Ficoll-70 w

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16

Nascimento, Carlos Antonio Do, Katalin Kauser та Gabor M. Rubanyi. "Effect of 17β-estradiol in hypercholesterolemic rabbits with severe endothelial dysfunction". American Journal of Physiology-Heart and Circulatory Physiology 276, № 5 (1999): H1788—H1794. http://dx.doi.org/10.1152/ajpheart.1999.276.5.h1788.

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17β-Estradiol prevents early vascular lesion development and may also affect advanced atherosclerosis. To test the antiatherosclerotic effect of estrogen under conditions that resemble more advanced human atherosclerosis with severe endothelial dysfunction, we have investigated the effect of 17β-estradiol in hypercholesterolemic rabbits treated with the nitric oxide synthase inhibitor N ω-nitro-l-arginine methyl ester (l-NAME). Chronicl-NAME administration attenuated endothelial nitric oxide (EDNO)-mediated vascular responses leading to significantly accelerated atherosclerotic plaque developm

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17

Xu, Shenghong, Ying Cheng, Janet R. Keast та Peregrine B. Osborne. "17β-Estradiol Activates Estrogen Receptor β-Signalling and Inhibits Transient Receptor Potential Vanilloid Receptor 1 Activation by Capsaicin in Adult Rat Nociceptor Neurons". Endocrinology 149, № 11 (2008): 5540–48. http://dx.doi.org/10.1210/en.2008-0278.

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There is mounting evidence that estrogens act directly on the nervous system to affect the severity of pain. Estrogen receptors (ERs) are expressed by sensory neurons, and in trigeminal ganglia, 17β-estradiol can indirectly enhance nociception by stimulating expression and release of prolactin, which increases phosphorylation of the nociceptor transducer transient receptor potential vanilloid receptor 1 (TRPV1). Here, we show that 17β-estradiol acts directly on dorsal root ganglion (DRG) sensory neurons to reduce TRPV1 activation by capsaicin. Capsaicin-induced cobalt uptake and the maximum TR

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18

Wang, X. H., and V. Ivanov. "Microbial structure of nitrifying granules and their estrogens degradation properties." Water Science and Technology 59, no. 9 (2009): 1855–62. http://dx.doi.org/10.2166/wst.2009.218.

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It has been known that endocrine disruption compounds such as natural estrogens estrone, 17β-estradiol, estriol, and synthetic steroid 17a-ethynylestradiol can be degraded by nitrifying bacteria. The aim of this research was to test biodegradation of estrogens by microbial granules containing nitrifying bacteria. Cultivation of microbial granules was performed in sequencing batch reactor in model wastewater with carbon to nitrogen ratio of 100:30 by weight. After the system reached the steady state, the mean diameter of granules, sludge volume index of granular biomass, and biomass concentrati

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19

Tanaka, H., Y. Yakou, A. Takahashi, T. Higashitani, and K. Komori. "Comparison between estrogenicities estimated from DNA recombinant yeast assay and from chemical analyses of endocrine disruptors during sewage treatment." Water Science and Technology 43, no. 2 (2001): 125–32. http://dx.doi.org/10.2166/wst.2001.0081.

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This study discusses the estrogenicity and the extent of estrogenic effects, of sewage and treated sewage in public sewage treatment plants in Japan. The estrogenicity in this study was measured with a DNA recombinant yeast strain. Using this method, 43 chemicals that are suspected to have estrogen-like effects were measured and their estrogenicities were evaluated in terms of 17β-estradiol equivalents by comparison with the estrogenicity of 17β-estradiol. 17β-estradiol equivalents of influent and effluent sampled from 20 sewage treatment plants (STPs) were measured with this method. Because t

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20

Simpkins, James W., Gopal Rajakumar, Yu-Qi Zhang, et al. "Estrogens may reduce mortality and ischemic damage caused by middle cerebral artery occlusion in the female rat." Journal of Neurosurgery 87, no. 5 (1997): 724–30. http://dx.doi.org/10.3171/jns.1997.87.5.0724.

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✓ The present study was undertaken to determine if estrogens protect female rats from the neurodegenerative effects of middle cerebral artery (MCA) occlusion. The rats were ovariectomized and 7 or 8 days later various estrogen preparations were administered before or after MCA occlusion. Pretreatment with 17β-estradiol (17β-E2) or a brain-targeted 17β-E2 chemical delivery system (CDS) decreased mortality from 65% in ovariectomized rats to 22% in 17β-E2—treated and 16% in 17β-E2 CDS—treated rats. This marked reduction in mortality was accompanied by a reduction in the ischemic area of the brain

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21

Kim, Jin Hyung, та Seung-Taek Lee. "Polyamine Oxidase Expression Is Downregulated by 17β-Estradiol via Estrogen Receptor 2 in Human MCF-7 Breast Cancer Cells". International Journal of Molecular Sciences 23, № 14 (2022): 7521. http://dx.doi.org/10.3390/ijms23147521.

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Polyamine levels decrease with menopause; however, little is known about the mechanisms regulated by menopause. In this study, we found that among the genes involved in the polyamine pathway, polyamine oxidase (PAOX) mRNA levels were the most significantly reduced by treatment with 17β-estradiol in estrogen receptor (ESR)-positive MCF-7 breast cancer cells. Treatment with 17β-estradiol also reduced the PAOX protein levels. Treatment with selective ESR antagonists and knockdown of ESR members revealed that estrogen receptor 2 (ESR2; also known as ERβ) was responsible for the repression of PAOX

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22

Hewitt, Kylie N., Kyriakos Pratis, Margaret E. E. Jones, and Evan R. Simpson. "Estrogen Replacement Reverses the Hepatic Steatosis Phenotype in the Male Aromatase Knockout Mouse." Endocrinology 145, no. 4 (2004): 1842–48. http://dx.doi.org/10.1210/en.2003-1369.

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Abstract The aromatase knockout (ArKO) mouse cannot synthesize endogenous estrogens due to a disruption to the Cyp19 gene. Previously we have shown both male and female ArKO mice have an age progressive obese phenotype and a sexually dimorphic disruption to hepatic cholesterol and triglyceride homeostasis. Only ArKO males have elevated hepatic triglyceride levels leading to hepatic steatosis partly due to an increase in expression of enzymes involved in de novo lipogenesis and transporters involved in fatty acid uptake. In this study ArKO males were treated with 17β-estradiol (3 μg/ kg·d) at 1

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23

Verdú, Elena F., Yikang Deng, Premysl Bercik, and Stephen M. Collins. "Modulatory effects of estrogen in two murine models of experimental colitis." American Journal of Physiology-Gastrointestinal and Liver Physiology 283, no. 1 (2002): G27—G36. http://dx.doi.org/10.1152/ajpgi.00460.2001.

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The association between oral contraceptives or pregnancy and inflammatory bowel disease is unclear. We investigated whether 17β-estradiol modulates intestinal inflammation in two models of colitis. Female mice were treated with 17β-estradiol alone or with tamoxifen, tamoxifen alone, 17α-estradiol, or placebo. Dinitrobenzene sulfonic acid (DNB)- or dextran sodium sulfate (DSS)-induced colitis were assessed macroscopically, histologically, and by myeloperoxidase (MPO) activity. Malondialdehyde and mRNA levels of intercellular adhesion molecule-1 (ICAM-1), interferon-γ (IFN-γ), and interleukin-13

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24

MacLusky, Neil J., Victoria N. Luine, Tibor Hajszan та Csaba Leranth. "The 17α and 17β Isomers of Estradiol Both Induce Rapid Spine Synapse Formation in the CA1 Hippocampal Subfield of Ovariectomized Female Rats". Endocrinology 146, № 1 (2005): 287–93. http://dx.doi.org/10.1210/en.2004-0730.

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Previous studies have demonstrated that estradiol-17β and estradiol-17α both induce short-latency effects on spatial memory in rats, estradiol-17α being at least as potent as its 17β isomer. To determine whether the mechanisms underlying these behavioral responses might include effects on hippocampal synaptic plasticity, CA1 pyramidal spine synapse density (PSSD) was measured in ovariectomized rats within the first few hours after sc estrogen injection. PSSD increased markedly (by 24%) 4.5 h after the administration of 45 μg/kg estradiol-17β. The PSSD response was significantly greater (44% ab

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Bhavnani, Bhagu R., Shui-Pang Tam та XiaoFeng Lu. "Structure Activity Relationships and Differential Interactions and Functional Activity of Various Equine Estrogens Mediated via Estrogen Receptors (ERs) ERα and ERβ". Endocrinology 149, № 10 (2008): 4857–70. http://dx.doi.org/10.1210/en.2008-0304.

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The human estrogen receptors (ERs) α and β interact with 17β-estradiol (17β-E2), estrone, 17α-estradiol, and the ring B unsaturated estrogens, equilin, 17β-dihydroequilin, 17α-dihydroequilin, equilenin, 17β-dihydroequilenin, 17α-dihydroequilenin, Δ8-estrone, and Δ8, 17β-E2 with varying affinities. In comparison to 17β-E2, the relative binding affinities of most ring B unsaturated estrogens were 2- to 8-fold lower for ERα and ERβ, however, some of these unique estrogens had two to four times greater affinity for ERβ than ERα. The transcriptional activity of these estrogens in HepG2 cells transf

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Surico, Daniela, Alfredo Ercoli, Serena Farruggio та ін. "Modulation of Oxidative Stress by 17 β-Estradiol and Genistein in Human Hepatic Cell Lines In Vitro". Cellular Physiology and Biochemistry 42, № 3 (2017): 1051–62. http://dx.doi.org/10.1159/000478752.

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Background/Aims: estrogens and phytoestrogens exert hepatoprotection through mechanisms not clearly examined yet. Here, we investigated the protective effects exerted by 17β-estradiol and genistein against oxidative stress in hepatocytes and hepatic stellate cells (HSCs) and the involvement of specific receptors and the intracellular signalling. Methods: Huh7.5 and LX-2, alone or in co-culture with Huh7.5, were treated with 17β-estradiol and genistein alone or in the presence of menadione and of estrogen receptors (ERs) and G protein-coupled-estrogenic-receptors (GPER) blockers. Cell viability

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27

Li, Jing, Byung Kun Kim, Kang-Kyun Wang, et al. "Sensing Estrogen with Electrochemical Impedance Spectroscopy." Journal of Analytical Methods in Chemistry 2016 (2016): 1–6. http://dx.doi.org/10.1155/2016/9081375.

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This study demonstrates the application feasibility of electrochemical impedance spectroscopy (EIS) in measuring estrogen (17β-estradiol) in gas phase. The present biosensor gives a linear response (R2=0.999) for 17β-estradiol vapor concentration from 3.7 ng/L to 3.7 × 10−4 ng/L with a limit of detection (3.7 × 10−4 ng/L). The results show that the fabricated biosensor demonstrates better detection limit of 17β-estradiol in gas phase than the previous report with GC-MS method. This estrogen biosensor has many potential applications for on-site detection of a variety of endocrine disrupting com

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Mukai, Kanae, Yukari Nakajima, Tamae Urai та ін. "The Effect of 17β-Estradiol Administration on Cutaneous Wound Healing in 24-Week Ovariectomized Female Mice". Journal of Hormones 2014 (21 січня 2014): 1–8. http://dx.doi.org/10.1155/2014/234632.

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Estrogen replacement promotes cutaneous wound healing in 8–10-week young ovariectomized female mice. However, research using aged ovariectomized female mice has not been reported, to the best of our knowledge. Therefore, we investigated the effect of 17β-estradiol on cutaneous wound healing using 24-week middle-aged ovariectomized female mice. Twenty-week-old female mice were divided into three groups: medication with 17β-estradiol after ovariectomy (OVX + 17β-estradiol), ovariectomy (OVX), and sham (SHAM). After 4 weeks, the mice received two full-thickness wounds. Then, the OVX + 17β-estradi

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Clarke, Scott D., Iain J. Clarke, Alexandra Rao, Roger G. Evans, and Belinda A. Henry. "Differential Effects of Acute and Chronic Estrogen Treatment on Thermogenic and Metabolic Pathways in Ovariectomized Sheep." Endocrinology 154, no. 1 (2013): 184–92. http://dx.doi.org/10.1210/en.2012-1758.

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Estrogen is protective against weight gain, but the underlying mechanisms are not fully elucidated. We sought to characterize the effects of estrogen on energy expenditure in skeletal muscle and adipose tissue in ovariectomized sheep. Temperature probes were implanted into sc (gluteal) and visceral (retroperitoneal) fat depots and skeletal muscle of the hind limb (vastus lateralis). Food was available from 1100–1600 h to entrain postprandial thermogenesis. We characterized the effects of single (50 μg estradiol benzoate, im) and repeated (25 μg estradiol-17β, iv) injections as well as chronic

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30

Ren, Jimin, Luis Rodriguez, Talon Johnson, Anke Henning та Yasin Y. Dhaher. "17β-Estradiol Effects in Skeletal Muscle: A 31P MR Spectroscopic Imaging (MRSI) Study of Young Females during Early Follicular (EF) and Peri-Ovulation (PO) Phases". Diagnostics 14, № 3 (2024): 235. http://dx.doi.org/10.3390/diagnostics14030235.

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The natural variation in estrogen secretion throughout the female menstrual cycle impacts various organs, including estrogen receptor (ER)-expressed skeletal muscle. Many women commonly experience increased fatigue or reduced energy levels in the days leading up to and during menstruation, when blood estrogen levels decline. Yet, it remains unclear whether endogenous 17β-estradiol, a major estrogen component, directly affects the energy metabolism in skeletal muscle due to the intricate and fluctuating nature of female hormones. In this study, we employed 2D 31P FID-MRSI at 7T to investigate p

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31

Flinsenberg, Thijs W. H., Saskia van der Sterren, Anne N. H. van Cleef, Marijn J. Schuurman, Pia Ågren, and Eduardo Villamor. "Effects of sex and estrogen on chicken ductus arteriosus reactivity." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 298, no. 5 (2010): R1217—R1224. http://dx.doi.org/10.1152/ajpregu.00839.2009.

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Sex hormones have an important influence on cardiovascular physiology and pathophysiology and sex differences in vascular reactivity have been widely demonstrated. In the present study we hypothesized 1) the presence of sexual dimorphism in chicken ductus arteriosus (DA) responsiveness to contractile and relaxant stimuli and 2) that estrogens are vasoactive in the chicken DA. In vitro contractions (assessed with a wire myograph) induced by normoxia, KCl, 4-aminopyridine, norepinephrine, phenylephrine, U46619, or endothelin-1, as well as relaxations induced by ACh, sodium nitroprusside, BAY 41–

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32

Lee, Jee Y., Soo Y. Choi, Tae H. Oh та Tae Y. Yune. "17β-Estradiol Inhibits Apoptotic Cell Death of Oligodendrocytes by Inhibiting RhoA-JNK3 Activation after Spinal Cord Injury". Endocrinology 153, № 8 (2012): 3815–27. http://dx.doi.org/10.1210/en.2012-1068.

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A delayed oligodendrocyte cell death after spinal cord injury (SCI) contributes to chronic demyelination of spared axons, leading to a permanent neurological deficit. Therefore, therapeutic approaches to prevent oligodendrocyte cell death after SCI should be considered. Estrogens are well known to have a broad neuroprotective effect, but the protective effect of estrogens on oligodendrocytes after injury is largely unknown. Here, we demonstrated that 17β-estradiol attenuates apoptosis of oligodendrocytes by inhibiting RhoA and c-Jun-N-terminal kinase activation after SCI. Estrogen receptor (ER

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33

Qian, Tianrun, Jia Bao, Xuepeng Liu, Gerile Oudeng та Weiwei Ye. "A “turn-on” fluorescence resonance energy transfer aptasensor based on carbon dots and gold nanoparticles for 17β-estradiol detection in sea salt". RSC Advances 13, № 40 (2023): 27772–81. http://dx.doi.org/10.1039/d3ra05410a.

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Анотація:

A “turn-on” FRET aptasensor for 17β-estradiol detection was developed. It can detect 17β-estradiol with high sensitivity and selectivity. It showed potential for estrogen detection in food safety and environmental applications.

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34

Nakrst, Jana, Mirjana Bistan, Tatjana Tišler, Jana Zagorc-Končan, Jan Derco, and Andreja Žgajnar Gotvajn. "Comparison of Fenton's oxidation and ozonation for removal of estrogens." Water Science and Technology 63, no. 10 (2011): 2131–37. http://dx.doi.org/10.2166/wst.2011.339.

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This study compares efficiency of Fenton's oxidation and ozonation of 17β-estradiol (E2) and 17α-ethinylestradiol (EE2) as two possible processes for removal of estrogens from aqueous solutions. The effectiveness of Fenton's oxidative removal was studied at different ratios of reagents Fe2+:H2O2 (1:0.5; 1:10; 1:20; 1:33), where with some molar ratios up to 100% removal of E2 and EE2 was achieved in the first few minutes of reaction. The best molar ratio for E2 (17β-estradiol) removal was 1:33, while in the case of EE2 the most efficient one was 1:20 ratio. Ozonation was much faster, because co

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35

Jalabert, Cecilia, Maria A. Shock, Chunqi Ma, and Kiran K. Soma. "LC-MS/MS for Ultra-Sensitive Quantification of Multiple Estrogens in the Blood and Brain." Journal of the Endocrine Society 5, Supplement_1 (2021): A542. http://dx.doi.org/10.1210/jendso/bvab048.1104.

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Abstract Estrogens are steroid hormones that affect many aspects of brain function, including cognition, social behavior, and neuroprotection. It is well-known that estrogens are synthesized in the ovaries. Estrogens are also synthesized in the brain, where aromatase is expressed in specific regions. Importantly, estrogens play crucial roles in the brain, even at extremely low levels. Current assays lack the necessary sensitivity and/or specificity to measure brain-synthesized estrogens. Furthermore, current methods focus on only 17β-estradiol and generally disregard other estrogens that are s

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36

Stefano, George B., Patrick Cadet, Christophe Breton, et al. "Estradiol-stimulated nitric oxide release in human granulocytes is dependent on intracellular calcium transients: evidence of a cell surface estrogen receptor." Blood 95, no. 12 (2000): 3951–58. http://dx.doi.org/10.1182/blood.v95.12.3951.

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Abstract We tested the hypothesis that estrogen acutely stimulates constitutive nitric oxide synthase activity in human granulocytes by acting on a cell surface estrogen receptor (ER). The release of nitric oxide was measured in real time with an amperometric probe. Exposure of granulocytes to 17β-estradiol stimulated NO release within seconds in a concentration-dependent manner. The NO release was also stimulated by 17β-estradiol conjugated to bovine serum albumin (E2-BSA), which suggests mediation by a cell surface receptor. Tamoxifen, an ER inhibitor, antagonized the action of both 17β-estr

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37

Stefano, George B., Patrick Cadet, Christophe Breton, et al. "Estradiol-stimulated nitric oxide release in human granulocytes is dependent on intracellular calcium transients: evidence of a cell surface estrogen receptor." Blood 95, no. 12 (2000): 3951–58. http://dx.doi.org/10.1182/blood.v95.12.3951.012k21_3951_3958.

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Анотація:

We tested the hypothesis that estrogen acutely stimulates constitutive nitric oxide synthase activity in human granulocytes by acting on a cell surface estrogen receptor (ER). The release of nitric oxide was measured in real time with an amperometric probe. Exposure of granulocytes to 17β-estradiol stimulated NO release within seconds in a concentration-dependent manner. The NO release was also stimulated by 17β-estradiol conjugated to bovine serum albumin (E2-BSA), which suggests mediation by a cell surface receptor. Tamoxifen, an ER inhibitor, antagonized the action of both 17β-estradiol and

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38

Nakamura, Takehiro, Ya Hua, Richard F. Keep, Jung-Weon Park, Guohua Xi, and Julian T. Hoff. "Estrogen therapy for experimental intracerebral hemorrhage in rats." Journal of Neurosurgery 103, no. 1 (2005): 97–103. http://dx.doi.org/10.3171/jns.2005.103.1.0097.

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Object The aims of this study were to determine the following: whether there are sex differences in intracerebral hemorrhage (ICH) induced brain injury in rats, whether delayed administration of 17β-estradiol can reduce ICH-induced brain damage, and whether these effects are estrogen receptor (ER)-dependent. Methods Male and female Sprague—Dawley rats received an infusion of 100 µl autologous whole blood into the right basal ganglia. Twenty-four hours later the rats were killed. The effects of 17β-estradiol on ICH-induced brain injury were examined by measuring brain edema and neurological def

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39

Palmon, Sally C., Megan J. Williams, Marguerite T. Littleton-Kearney, Richard J. Traystman, Danuta Kosk-Kosicka, and Patricia D. Hurn. "Estrogen Increases cGMP in Selected Brain Regions and in Cerebral Microvessels." Journal of Cerebral Blood Flow & Metabolism 18, no. 11 (1998): 1248–52. http://dx.doi.org/10.1097/00004647-199811000-00011.

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We have previously reported that exogenous and endogenous estrogen can amplify residual cerebral blood flow during experimental cerebral ischemia. Because estrogen has been linked to nitric oxide and cyclic guanosine monophosphate (cGMP) signaling in noncerebral tissue, we tested the hypothesis that long-term 17β-estradiol treatment increases basal cGMP in brain homogenates and cerebral microvessels in female rabbits. We also determined whether there are important baseline gender-specific differences in regional cGMP. Adult female rabbits were implanted with 17β-estradiol pellets, 10 mg (F10,

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40

Elzer, Joachim G., Sajjad Muhammad, Tim M. Wintermantel та ін. "Neuronal Estrogen Receptor-α Mediates Neuroprotection by 17β-Estradiol". Journal of Cerebral Blood Flow & Metabolism 30, № 5 (2009): 935–42. http://dx.doi.org/10.1038/jcbfm.2009.258.

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17β-Estradiol (E2) was shown to exert neuroprotective effects both in in vitro and in vivo models of stroke. Although these effects of E2 are known to require estrogen receptor-α (ERα), the cellular target of estrogen-mediated neuroprotection remains unknown. Using cell type-specific ER mutant mice in an in vivo model of stroke, we specifically investigated the role of ERα in neuronal cells versus its role in the microglia in the mediation of neuroprotection by estrogens. We generated and analyzed two different tissue-specific knockout mouse lines lacking ERα either in cells of myeloid lineage

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41

Jayachandran, Muthuvel, Toshio Hayashi, Daigo Sumi, Akihisa Iguchi та Virginia M. Miller. "Temporal effects of 17β-estradiol on caveolin-1 mRNA and protein in bovine aortic endothelial cells". American Journal of Physiology-Heart and Circulatory Physiology 281, № 3 (2001): H1327—H1333. http://dx.doi.org/10.1152/ajpheart.2001.281.3.h1327.

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Анотація:

Endothelial nitric oxide synthase (eNOS) is regulated both by caveolin-1 and 17β-estradiol (E2). Temporal relationships between effects of estrogen on caveolin-1 and nitric oxide (NO) are not known. Therefore, this study was designed to determine whether estrogen regulates caveolin-1 and, if so, whether such regulation corresponds to changes in nitrite/nitrate (NOx) production. Bovine aortic endothelial cells (BAECs) were cultured in the absence and presence of 17β-estradiol or 17α-estradiol (10−8 and 10−10 M) for 12, 24, and 48 h. eNOS protein expression and NOx production increased significa

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42

Kuiper, George G. J. M., Bo Carlsson, Kaj Grandien та ін. "Comparison of the Ligand Binding Specificity and Transcript Tissue Distribution of Estrogen Receptors α and β". Endocrinology 138, № 3 (1997): 863–70. http://dx.doi.org/10.1210/endo.138.3.4979.

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Abstract The rat estrogen receptor (ER) exists as two subtypes, ERα and ERβ, which differ in the C-terminal ligand binding domain and in the N-terminal transactivation domain. In this study we investigated the messenger RNA expression of both ER subtypes in rat tissues by RT-PCR and compared the ligand binding specificity of the ER subtypes. Saturation ligand binding analysis of in vitro synthesized human ERα and rat ERβ protein revealed a single binding component for 16α-iodo-17β-estradiol with high affinity[ dissociation constant (Kd) = 0.1 nm for ERα protein and 0.4 nm for ERβ protein]. Mos

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43

Alzamora, Rodrigo, Laura R. Brown та Brian J. Harvey. "Direct Binding and Activation of Protein Kinase C Isoforms by Aldosterone and 17β-Estradiol". Molecular Endocrinology 21, № 11 (2007): 2637–50. http://dx.doi.org/10.1210/me.2006-0559.

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Abstract Protein kinase C (PKC) is a signal transduction protein that has been proposed to mediate rapid responses to steroid hormones. Previously, we have shown aldosterone directly activates PKCα whereas 17β-estradiol activates PKCα and PKCδ; however, neither the binding to PKCs nor the mechanism of action has been established. To determine the domains of PKCα and PKCδ involved in binding of aldosterone and 17β-estradiol, glutathione S-transferase fusion recombinant PKCα and PKCδ mutants were used to perform in vitro binding assays with [3H]aldosterone and [3H]17β-estradiol. 17β-Estradiol bo

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44

Mukai, Kanae, Yuriko Miyasaka, Kana Takata, et al. "Comparison of the Cutaneous Wound Healing of Ovariectomized Mouse at 12 Weeks with That of SHAM and Estrogen-Administered Mice." Journal of Hormones 2014 (July 7, 2014): 1–6. http://dx.doi.org/10.1155/2014/484258.

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The aim of this experiment was to investigate the effect of 17β-estradiol on cutaneous wound healing in 12-week ovariectomized (OVX) female mice. Eight-week-old female mice were divided into three groups: administration of 17β-estradiol after OVX (OVX + 17β-estradiol), OVX, and sham (SHAM). Four weeks after surgery, the mice received two full-thickness cutaneous wounds. 17β-Estradiol at 0.01 g/day was administered on the backs of mice in the OVX + 17β-estradiol group every day. Plasma 17β-estradiol level in the OVX + 17β-estradiol group was thus significantly higher than in the SHAM and OVX gr

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45

Canesi, Laura, Caterina Ciacci, Lucia Cecilia Lorusso та ін. "Immunomodulation by 17β-estradiol in bivalve hemocytes". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, № 3 (2006): R664—R673. http://dx.doi.org/10.1152/ajpregu.00139.2006.

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In mammals, estrogens have dose- and cell-type-specific effects on immune cells and may act as pro- and anti-inflammatory stimuli, depending on the setting. In the bivalve mollusc Mytilus, the natural estrogen 17β-estradiol (E2) has been shown to affect neuroimmune functions. We have investigated the immunomodulatory role of E2 in Mytilus hemocytes, the cells responsible for the innate immune response. E2 at 5–25 nM rapidly stimulated phagocytosis and oxyradical production in vitro; higher concentrations of E2 inhibited phagocytosis. E2-induced oxidative burst was prevented by the nitric oxide

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46

Bracamonte, M. P., M. Jayachandran, K. S. Rud та V. M. Miller. "Acute effects of 17β-estradiol on femoral veins from adult gonadally intact and ovariectomized female pigs". American Journal of Physiology-Heart and Circulatory Physiology 283, № 6 (2002): H2389—H2396. http://dx.doi.org/10.1152/ajpheart.00184.2002.

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Our experiments were designed to determine the acute effects of 17β-estradiol on femoral veins from intact and ovariectomized female pigs. Rings of femoral veins with or without endothelium were suspended in organ chambers for measurement of isometric force. Concentration-response curves to 17β-estradiol (10−9 to 10−5 M) were obtained in veins contracted with prostaglandin F2α in the absence and presence of inhibitors of either estrogen receptors (ICI-182780; 10−5 M), nitric oxide synthase [ N G-monomethyl-l-arginine (l-NMMA); 10−4 M], soluble guanylate cyclase (1- H-[1,2,4]oxadiazolo[4,3-a]qu

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Deng, Zhiqin, Shuang Peng, Yanfang Zheng та ін. "Estradiol activates chloride channels via estrogen receptor-α in the cell membranes of osteoblasts". American Journal of Physiology-Cell Physiology 313, № 2 (2017): C162—C172. http://dx.doi.org/10.1152/ajpcell.00014.2017.

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Estrogen plays important roles in regulation of bone formation. Cl− channels in the ClC family are expressed in osteoblasts and are associated with bone physiology and pathology, but the relationship between Cl− channels and estrogen is not clear. In this study the action of estrogen on Cl− channels was investigated in the MC3T3-E1 osteoblast cell line. Our results show that 17β-estradiol could activate a current that reversed at a potential close to the Cl− equilibrium potential, with a sequence of anion selectivity of I− > Br− > Cl− > gluconate, and was inhibited by the Cl− channel

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Nekooeian, Ali Akbar, and Catherine C. Y. Pang. "Effects of estrogen on venous function in rats with chronic heart failure." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 6 (2000): H1941—H1947. http://dx.doi.org/10.1152/ajpheart.2000.278.6.h1941.

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The effect of 17β-estradiol on venous function was investigated in ovariectomized rats with heart failure. Rats (50–60 days old) were ovariectomized and implanted with 60-day-release pellets that contain 17β-estradiol (1.5 mg) or vehicle. The left coronary artery was ligated 7 days later. Another group of ovariectomized rats was given vehicle pellets and then a sham operation was performed. The rats were studied while under pentobarbital anesthesia at 7 wk after ligation. Ligated rats, relative to sham groups, had lower mean arterial pressure (MAP, −34 mmHg) and cardiac output (CO, −38%); high

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Eid, A. H., K. Maiti, S. Mitra та ін. "Estrogen increases smooth muscle expression of α2C-adrenoceptors and cold-induced constriction of cutaneous arteries". American Journal of Physiology-Heart and Circulatory Physiology 293, № 3 (2007): H1955—H1961. http://dx.doi.org/10.1152/ajpheart.00306.2007.

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Анотація:

Raynaud's phenomenon, which is characterized by intense cold-induced constriction of cutaneous arteries, is more common in women compared with men. Cold-induced constriction is mediated in part by enhanced activity of α2C-adrenoceptors (α2C-ARs) located on vascular smooth muscle cells (VSMs). Experiments were therefore performed to determine whether 17β-estradiol regulates α2C-AR expression and function in cutaneous VSMs. 17β-Estradiol (0.01–10 nmol/l) increased expression of the α2C-AR protein and the activity of the α2C-AR gene promoter in human cultured dermal VSMs, which was assessed follo

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50

Binko, J., та H. Majewski. "17β-Estradiol reduces vasoconstriction in endothelium-denuded rat aortas through inducible NOS". American Journal of Physiology-Heart and Circulatory Physiology 274, № 3 (1998): H853—H859. http://dx.doi.org/10.1152/ajpheart.1998.274.3.h853.

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Анотація:

Estrogen produces vasodilatation through the induction of nitric oxide synthase (NOS) in the endothelium, but there are many reports of endothelium-independent effects. In the present study, these processes were investigated in rat aortas isolated from ovariectomized rats. Long-term in vitro treatment with 17β-estradiol (10 nM for 24 h) in an organ culture system slightly reduced acetylcholine-mediated vasorelaxation in endothelium-intact aortic rings. 17β-Estradiol (1 and 10 nM for 24 h) also attenuated the phenylephrine-induced constriction in endothelium-denuded aortas, and this effect was

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