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Results for “Estrogen Receptor beta”

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At least 19 recordsLinked to original sources
PubMed1979

Relationship between estrogen receptors, 17 beta-hydroxysteroid dehydrogenase and estrogen content in human breast cancer.

Estrone and estradiol levels in tumor tissue cytosols were determined in 11 premenopausal and 20 postmenopausal women at the same time that 17 beta-hydroxysteroid dehydrogenase and estrogen receptors (ER) were carried out on their breast cancers. Estrogen receptor positive tumors showed significantly higher levels of estrone and estradiol. However, all ER negative tumors contained measurable amounts of both estradiol and estrone. Higher levels of estrone were observed in ER negative tumors which correlates well with high 17 beta-hydroxysteroid dehydrogenase activity. These results suggest that false negative receptor assays in the premenopausal women is not likely to be due to occupancy of receptors by endogenous estrogens. Furthermore, the higher estrone content in the ER negative group is probably due to high 17 beta-hydroxysteroid dehydrogenase activity inherent to these tumor cells.

17-Hydroxysteroid Dehydrogenases↗
PubMed2026

The role of estrogen receptors and house dust mite-induced DNA methylation in a mouse model.

Asthma is a chronic respiratory disease affecting over 230 million people worldwide, with higher prevalence in women. Environmental allergens such as house dust mite (HDM) trigger airway inflammation and hyperresponsiveness (AHR), yet the epigenetic mechanisms underlying these responses remain poorly understood. Furthermore, the role of estrogen receptors in the context of asthma is understudied. We aimed to investigate whether estrogen receptor-specific DNA methylation contributes to HDM-induced airway remodeling and hyperresponsiveness. Male and female C57BL/6J wild-type mice and estrogen receptor &#x3b1; and &#x3b2; knockout mice (Esr1-/- and Esr2-/-) were exposed to HDM or phosphate-buffered saline for 5 wk. DNA methylation and RNA sequencing data were obtained from snap-frozen whole lung tissues. HDM exposure resulted in widespread differential methylation of genes associated with inflammation and AHR, including Itgal, Tmem267, Rap1b, Bmf, Mid1, Fgd1, Ddx4, Comtd1, Filip1l, Grb10, and Chst7. Notably, the absence of estrogen receptor &#x3b2; (in Esr2-/- mice) produced the most pronounced methylation patterns, particularly in females. Pathway enrichment analysis revealed asthma-relevant processes such as extracellular matrix remodeling, leukocyte adhesion and migration, airway smooth muscle contraction, and inflammatory signaling. Integration of methylation and gene expression data confirmed significant correlations (P < 0.05) for Itgal, Rap1b, and Tmem267, and a marginal correlation for Chst7 (P < 0.1), implicating these genes in allergic asthma pathogenesis. Our findings demonstrate that HDM exposure induces sex-specific epigenetic changes mediated by estrogen receptor status, highlighting a potential mechanism for increased asthma susceptibility in women. These results can inform estrogen receptor-targeted treatment strategies for allergic airway diseases.NEW & NOTEWORTHY Understanding estrogen receptor-mediated epigenetic regulation provides a foundation for developing sex-specific interventions for asthma, addressing the higher prevalence and severity observed in women. In this study, we demonstrate that exposure to house dust mite in the mouse lung is associated with epigenetic alterations in genes linked to airway hyperresponsiveness and lung inflammation. These alterations were dependent on the presence or absence of estrogen receptors.

Animals↗
PubMed2026

Exploring the potential mechanism of Huang'e capsule against spontaneous benign prostatic hyperplasia in beagle dogs using high-performance liquid chromatography-quadrupole-time-of-flight tandem mass spectrometry, gas chromatography-mass spectrometry, and network pharmacology.

OBJECTIVE: To investigate the therapeutic efficacy and potential mechanisms of Huang'e capsule (, HEC) against benign prostatic hyperplasia (BPH). METHODS: The chemical profile of HEC was characterized using high-performance liquid chromatographyquadrupole-time-of-flight tandem mass spectrometry (HPLC-Q-TOF-MS/MS) and gas chromatography-mass spectrometry (GC-MS) techniques. Network pharmacology was employed to analyze potential active compounds, core targets, and key signaling pathways. A spontaneous canine BPH model was used to evaluate the efficacy of HEC and to validate the predictions from network pharmacology. RESULTS: A total of 51 chemical components of HEC were identified, comprising 19 from HPLC-Q-TOF-MS/MS and 32 from GC-MS analyses. The "components-targets-pathways-disease" network analysis predicted active compounds including (s)-coriolic acid, ethyl linoleate, peroxysimulenoline, physcion, and kaempferol. Core targets identified included cytochrome P450 family 19 subfamily A member 1, estrogen receptor 2 (ESR2), ESR1, and androgen receptor (AR). Kyoto Encyclopedia of Genes and Genomes enrichment analysis suggested that HEC's effects on BPH involve pathways related to cancer, phosphatidylinositol 3-kinase (PI3K) -protein kinase B (Akt)-signaling, proteoglycans in cancer, and prostate cancer signaling. Animal experiments showed that HEC significantly improved maximum urinary flow rates, reduced prostate weight, volume, and prostate index, and ameliorated histopathological changes. HEC regulated the balance between apoptosis and proliferation by downregulating AR and estrogen receptor alpha expression, while upregulating estrogen receptor beta expression. CONCLUSION: These findings indicate that HEC effectively ameliorates spontaneous BPH in beagle dogs, likely by regulating the balance between cell apoptosis and proliferation through multiple signaling pathways.

Animals↗
PubMed1979

Short-term tissue culture of human breast cancer: presence of estrogen receptors and 17 beta-estradiol stimulation of RNA synthesis.

The stimulation of RNA synthesis induced by estradiol has been studied on 60 breast cancers in short-term cultures. In the same tumors the estrogen receptor (ER) assay was carried out. In 35% of the cases studied the stimulating effect by estradiol in vitro was observed. The frequency of response to in vitro hormone treatment was higher (42%) in ER+ cancers and lower (25%) in ER- cancers. The specificity of the in vitro test was assessed by the use of tamoxifen.

Breast Neoplasms↗
PubMed2026

Mechanism of Shoutai Wan against recurrent spontaneous abortion: regulation of decidual vascular remodeling via ER&#x3b2;-ANGPT2 signaling axis.

Shoutai Wan (STW), a classic traditional Chinese medicine formula used to tonify the kidney and prevent miscarriage, has been widely applied in the clinical management of recurrent spontaneous abortion (RSA). Increasing clinical evidence supports its efficacy in reducing miscarriage rates and improving pregnancy outcomes. However, the molecular basis by which STW alleviates defective decidual vascular remodeling in unexplained RSA remains insufficiently understood. Clinically, decidual ER&#x3b2; and ANGPT2 expression, as well as serum estradiol, ANGPT2 and VEGFA levels were significantly decreased in RSA patients, accompanied by reduced decidual microvascular density. Furthermore, ER&#x3b2; expression was positively correlated with ANGPT2 and microvascular density. In vivo, STW dose-dependently reduced embryo loss in RSA mice, repaired the damaged decidual-placental interface structure, and improved vascular maturation, structural stability and endothelial-pericyte ultrastructural connections. Mechanistically, STW upregulated ER&#x3b2; expression. We demonstrated that ER&#x3b2; binds to the ANGPT2 promoter, suggesting transcriptional upregulation of ANGPT2, thereby activating Tie2 and the downstream PI3K/AKT pathway and increasing NO and VEGFA secretion. In vitro, hypoxia inhibited ER&#x3b2; nuclear translocation and ANGPT2 secretion in mDSCs, while STW-containing serum reversed these abnormalities. ER&#x3b2; knockdown impaired the pro-angiogenic capacity of mDSCs, which was partially rescued by exogenous ANGPT2 supplementation. Network pharmacology predicted that STW targets were mainly enriched in PI3K-Akt, estrogen, VEGF and angiogenesis-related pathways. Transcriptomic GSEA further revealed that the gene signatures of angiogenesis and PI3K-Akt signaling were markedly suppressed in the RSA model, and STW treatment significantly normalized these transcriptional signatures.

Female↗
PubMed1979

Steroid receptor levels and histology of endometriosis and adenomyosis.

Steroid receptors in endometriosis and adenomyosis were investigated to clarify their clinical significance. The receptor levels were determined by Scatchard plot analysis (4 degrees C, by dextran-coated charcoal). In the cytosols of both tissues, the 17 beta-estradiol-estrogen receptor (ER) complex demonstrated a dissociation constant (Kd) of 4.5 x 10(-10) M; the Kd of the progesterone-progesterone receptor (PR) complex was 1.5 x 10(-9) M; and the Kd of the dihydrotestosterone-androgen receptor (AR) complex was 4.0 x 10(-10) M. Seven cases of ovarian endometriosis were studied. The ER and PR levels in endometriosis seemed to be lower than those in the corresponding normal endometrium. AR was also present. There was a suggestion that most endometriosis is least responsive to progestogens. Ten cases of adenomyosis were studied. Histologic dating revealed a delay in the most aberrant endometrial tissue in adenomyosis, as compared with dating of corresponding normal endometrial tissue. ER and AR were detected in all cases. PR was not detected in some cases and, when detected, the content seemed to be lower, possibly suggesting the delayed dating.

Cytosol↗
PubMed1979

Decrease of estrogen receptors induced by 17 beta-estradiol and progesterone in cultured rabbit endometrial cells.

A whole cell technique to measure estradiol receptors in cultured rabbit endometrial cells is described. The estradiol receptors measured appear to be composed of at least two components: one component has high affinity but low capacity, while the other component has low affinity but high capacity. Using the assay, the effects of estradiol and progesterone pretreatment were examined on the estradiol receptor levels. It was found that both of the hormones decreased the number of estrogen receptors in the cultured cells. The finding that estradiol decreased its own receptors was unexpected and its possible relevance is discussed.

Animals↗
PubMed1979

Failure of rotenone to interfere with 17 beta-estradiol action in the rat uterus.

The involvement of rotenone in rat mammary carcinogenesis has been suggested to occur through estrogenic effects. This hypothesis was tested by determining the extent of rotenone inhibition of 17 beta-estradiol binding to the estrogen receptor and of the 17 beta-estradiol-induced uterotrophic response in ovariectomized Sprague-Dawley rats. Estradiol binding to the uterine estrogen receptor in the presence of rotenone was determined by charcoal assay and Scatchard analysis. Additionally, 17 beta-estradiol-receptor interactions were assessed on sucrose density gradients. No inhibition of binding was observed in either assay with ratios of rotenone/17 beta-estradiol in excess of 10,000. Finally, an in vivo approach was used to extend the in vitro data. Silastic capsules containing rotenone or 17 beta-estradiol were implanted in various combinations into eight groups of ovariectomized Sprague-Dawley rats (four rats/group). After five days, uteri were removed and weighed. An analysis of variance revealed that rotenone neither interfered with 17 beta-estradiol-induced uterine weight gain nor displayed any uterotrophic properties by itself. Results from these three procedures demonstrate that rotenone does not act as an estrogen or as an estrogen antagonist. Additionally, there were no other effects attributable to rotenone.

Animals↗
PubMed1979

Estrogens increase the number of thyrotropin-releasing hormone receptors on mammotropic cells in culture.

The number of plasma membrane receptors for TRH on tumor-derived mammotropic cells in culture, GH3 and GC cells, but not their affinity for TRH, was increased by estrogens. For GH3 cells, exposure to 10 nM 17 beta-estradiol for 48 h increased the receptor level from 54,000 to 90,000 sites/cell, while for GC cells, the number of receptors increased from 29,000 to 46,000 after 28 h. PRL accumulation in the medium was also increased by 17 beta-estradiol. 17 beta-Estradiol and diethylstilbestrol were equally potent in increasing the TRH receptor level, while estrone was only 1/10th as potent. Diethylstilbestrol bound to the cytoplasmic estrogen receptor with an apparent affinity approximately 2.5 times higher than 17 beta-estradiol in GH3 and GC cells, while the affinity for estrone was only 1/12th to 1/20th that of 17 beta-estradiol. Tamoxifen, an antiestrogenic compound, inhibited the increase in TRH receptor number induced by 0.3 nM 17 beta-estradiol and was capable of binding to the estrogen receptor. Modulation of the TRH receptor level on mammotropic cells by estrogens, which is likely mediated through cytoplasmic estrogen receptors, may be an important mechanism for regulation of TRH action.

Cell Line↗
PubMed1978

Effect of colchicine on estrogen action. II. Translocation of 17 beta-estradiol cytosol receptor complex into the nucleus.

Colchicine has previously been shown in our laboratory to inhibit 17 beta-estradiol stimulation of uterine water uptake in the immature rat measured 6 h after administration of the agents. We sought to determine whether this effect was mediated through colchicine action on translocation of estradiol receptor complex into the uterine cell nucleus. The time course of estradiol effect on uterine water uptake was followed with and without concurrent colchicine administration up to 6 h after administration. At no time during this period did there appear to be any influence of colchicine on translocation of the estradiol receptor complex into the nucleus. Examination of physical chemical characteristics of the nuclear estradiol receptr complex after estradiol and estradiol plus colchicine treatments revealed no observable differences. Thus, colchicine inhibition of estradiol-stimulated uterine water retention does not appear to be mediated through inhibition of nuclear translocation of estradiol-receptor complex nor to be due to any reduced retention time of estradiol-receptor complex in uterine nuclei.

Animals↗
PubMed1979

Estrogen receptor assay of mammary carcinomas. Effects of testosterone-estradiol-binding globulin (TeBG) and serum estradiol-17 beta.

To test the hypothesis that the serum sex steroid-binding protein, TeBG, might contaminate mammary carcinoma cytosols sufficiently to interfere with assay for estrogen receptor (ER), studies of tritiated estradiol-17 beta (3H-E2) binding were done following saturation with steroid hormones or after heat treatment of cytosol. Cytosols with appreciable 3H-E2 binding consistently showed a high degree of saturability with nonradioactive E2 and diethylstilbestrol (DES), and much less saturability with 5 alpha-dihydrotestosterone (DHT). Furthermore, they manifested heat-lability of 3H-E2 binding. These characteristics indicated that little, if any, TeBG was being detected in most cytosols, and that the amounts of TeBG present were not sufficient to interfere with the ER assay. Study of the relationship between serum E2 concentration at time of removal of the carcinoma and results of ER assay confirmed the need to interpret negative ER assays obtained for premenopausal women cautiously when serum E2 levels exceed approximately 300 pg/ml.

Adult↗
PubMedDate not supplied

Role of sulfate conjugation in estrogen metabolism and activity.

There has been an increasing interest in the sulfate conjugates of estrogens as important metabolites in steroid hormone homeostasis and activity. In women estrogen sulfates have been known as major components of plasma originating from ovarian secretion and hepatic metabolism. However, only recently has the capacity to sulfurylate estrogens been demonstrated in estrogen target tissues. Porcine uterus estrogen sulfotransferase appears only after the first complete estrous cycle. Following puberty, gilt uterine sulfurylation of estrogens is extremely active during diestrus, whereas estrogen sulfotransferase is not present during estrus. This cycling of estrogen sulfurylation in porcine and human uteri can be related directly to plasma progesterone levels. Rodent and human mammary tumors are also highly active in both steroid alcohol and estrogen sulfotransferases. Unlike uterine sulfotransferases, these enzymes are apparently stimulated by factors that appear following ovariectomy. The function of estrogen sulfurylation by target tissues remains obscure. However, recent investigations have indicated that the cyclic variation in endometrial estrogen sulfurylation may control the availability of 17 beta-estradiol to the cytoplasmic receptor. This premise is supported by the continued high estrogen sulfurylation activity and low nuclear receptor levels during implantation in fertilized gilts and sows. Utilizing purified bovine adrenal sulfotransferase, the substrate and inhibitor requirements were determined for this enzymes. It was also possible to design a specific inhibitor that will block estrogen sulfurylation without interfering with the receptor binding and nuclear migration of physiological levels of 17 beta-estradiol. This inhibitor, 3-methoxy-4-nitroestrone, will help in establishing the role of uterine and mammary estrogen sulfurylation.

Animals↗
PubMed1979

Properties of nuclear and cytoplasmic estrogen receptor in the rabbit corpus luteum: evidence for translocation.

Nuclear and cytoplasmic estrogen receptors have been identified and characterized in the rabbit corpus luteum, and validated methods are described for the measurement of both unoccupied and total estrogen receptor. Binding was specific for the biologically active estrogens. Equilibrium binding analysis of cytoplasmic estrogen receptor yielded saturable, high affinity binding sites with a Kd of 5.4 x 10(-11) M. Two types of binding sites were found in the nuclear fraction: one with high affinity (Kd = 8.9 x 10(-11) M) and low capacity, the other with low affinity (Kd = 2.7 x 10(-8) M) and high capacity. In the presence of 0.4 M KCl, the sedimentation coefficients of nuclear and cytoplasmic estrogen receptors are 3.4S, while the value is 6.8S for cytoplasmic receptor in buffer without KCl. Twenty minutes after an iv injection of 2 micrograms 17 beta-estradiol, the available and total cytoplasmic estrogen receptors were depleted. This depletion was accompanied by concomitant and stoichiometric accumulation of receptor in the nucleus, indicating an apparent translocation of the receptor. In corpora lutea of normal rabbits, approximately 80% of the total nuclear receptor is unoccupied. Evidence is presented to suggest that nuclear receptor sites might be ordinarily occupied with estradiol, but during isolation of the nuclear fraction these sites become available or unoccupied. The identification of nuclear estrogen receptor and the phenomenon of translocation of cytoplasmic receptor to the nucleus suggest a similarity of estrogen action in the rabbit corpus luteum and other estrogen target tissues.

Animals↗