• Title/Summary/Keyword: Progesterone receptor

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A Case of Canine Uterine Adenocarcinoma with Negative Estrogen and Progesterone Receptor Expression (개의 에스트로겐과 프로케스테론 수용체 발현이 되지 않은 자궁 선암종 증례)

  • Cho, Hyang-Mi;Kim, Hyun-Wook;Kim, Hye-Jin;Choi, Ji-Hye;Jang, Jae-Young;Choi, Ul-Soo
    • Journal of Veterinary Clinics
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    • v.28 no.3
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    • pp.303-306
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    • 2011
  • A 12-year-old female mixed breed dog receiving a progesterone drug was referred for evaluation of an abdominal mass. Abdominal radiography and ultrasonography revealed a swollen uterus and an associated mass. Serum chemistry revealed hyperglobulinemia consistent with acute inflammation based on the results of serum protein electrophoresis. Fine needle aspiration of the mass guided by ultrasonography was performed for cytological evaluation. The cytological impression was consistent with adenocarcinoma. Exploratory laparotomy identified a uterine body mass, which was surgically removed for histopathology. Histology of the mass identified a uterine adenocarcinoma. Immunochemistry using anti-estrogen and progesterone receptor antibodies was performed and neoplastic cells were negative to both antibodies while some normal elements were reactive to both of them. Computer tomography demonstrated evidence of metastatic disease in the lung one week after the surgery and the dog died about 40 days after surgery.

Effects of Exogenous Oxytocin on Steroid Hormones and Oxytocin Receptor Concentrations in Pregnant Rats (Oxytocin 투여가 임신 Rat의 Steroid Hormones 및 Oxytocin Receptors 농도에 미치는 영향)

  • 박용수;조현수;변명대
    • Korean Journal of Animal Reproduction
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    • v.26 no.2
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    • pp.183-192
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    • 2002
  • The present studies were carried out to examine the effects of exogenous oxytocin(OT) on plasma, uterine and placenta of estradiol-17$\beta$, progesterone, prostaglandin F$_2$$_{\alpha}$ (PGF$_2$$_{\alpha}$), Prostaglandin E$_2$(PGE$_2$) and OT receptor concentrations in pregnant rats. Pregnant rats received an injection of exogenous OT on days 14, 16, 18, 20, 22 of pregnancy and day 1 of postpartum. Concentrations of plasma estradiol-17 $\beta$ after OT injection started to increase after day 18 and peaked on day 22 of pregnancy but decreased on day 1 of postpartum. Plasma progesterone concentrations declined gradually from day 18 of pregnancy and decreased more rapidly until postpartum 1 day. Concentrations of estradiol-17$\beta$in uterine tissues after OT injection were sharply increased from day 20 to 22 of pregnancy and progestrone concentrations were peaked on day 16 and decreased rapidly from day 16 to 20 and maintained the same level until day 1 of postpartum. Uterine concentrations of PGF$_2$$_{\alpha}$ and PGE$_2$increased gradually until day 20 and peaked on day 22 of pregnancy but showed a marked decrease on day 1 of postpartum. Concentrations of PGF$_2$$_{\alpha}$ in placental tissues increased rapidly from day 14 of pregnancy and decreased sharply on day 1 of postpartum. Concentrations of PGE$_2$increased gradually after day 14 and peaked on day 20 of pregnancy. The concentration of OT receptor in uterus was significantly elevated from day 20 and rose to maximum on day 22 of pregnancy. These findings show that OT suppress the concentration of progestrone and stimulate productions of estradiol-17 $\beta$, PGF$_2$$_{\alpha}$, PGE$_2$ and oxytocin receptor concentrations in pregnant rats.

Role of estrogen and RAS signaling in repeated implantation failure

  • Hong, Kwonho;Choi, Youngsok
    • BMB Reports
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    • v.51 no.5
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    • pp.225-229
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    • 2018
  • In humans, hormonal regulation is crucial for the preparation of uterine environment leading to either successful implantation or menstrual cycle. Estrogen is a pivotal female steroid hormone that regulates the uterine dynamics along with progesterone in the estrous and menstrual cycles in humans. Estrogen signals act via nuclear estrogen receptor or membrane-bound receptor. The membrane-bound estrogen receptor plays a crucial role in the rapid response of estrogen in the uterine epithelium. Recently, RASD1 has received attention as a novel signal transducer of estrogen in various systems including female reproductive organs. In this review, we discuss the regulation of estrogen and RASD1 signaling in the uterus and also provide insights into RAS as a novel signaling molecule in repeated implantation failure.

Prophylactic Mastectomy and Implant-Based Breast Reconstruction of BRCA1/2 Mutation-Positive Patients in Korea

  • Lee, Joon Seok;Lee, Jeeyeon;Park, Ho Yong;Yang, Jung Dug
    • Journal of Interdisciplinary Genomics
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    • v.4 no.1
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    • pp.1-6
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    • 2022
  • Purpose: Mastectomy is performed as a surgical treatment for patients with breast cancer who have the BRCA 1/2 mutation. In this study, we have reported the trends in Korea for both immediate breast reconstruction and prophylactic mastectomy. Methods: This retrospective study was conducted from 2019 to 2021. Both skin-sparing mastectomy and immediate implant-based breast reconstruction with prepectoral and/or subpectoral techniques were performed in five patients with BRCA 1/2 mutations. Data on age; body mass index; cancer stage; BRCA 1/2 mutation; estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2 expression; diagnosis; and complications were collected. Results: The average (±standard deviation [SD]) age was 44.0±6.48 years old; BMI 24.5±2.25 kg/m2; and breast volumes were 365.8±70.34 and 382.4±96.33 cc for right and left ones, respectively. The BRCA 1 and 2 were diagnosed in four and one patients, respectively. The estrogen and progesterone receptors and human epidermal growth factor receptor 2 were detected in one (20%), one (20%), and three (60%) patients, respectively. The applied implant-based breast reconstruction techniques for ten breasts were subpectoral technique (n=7, 70%) and prepectoral technique (n=3, 30%). For the cancer stage, those with I, II, and III stages were one (20%), two (40%), and one (20%), respectively. There were no major complications such as Infection, seroma. Conclusion: When mastectomy is performed as surgical treatment in BRCA 1/2 mutation positive breast cancer patients, it is possible to obtain a better outcome with both implant-based breast reconstruction and different circumstances between breast cancer and contralateral breast.

Action Mechanism of Antiestrogens on Uterine Growth in Immature Rats (자궁세포 성장에 미치는 항에스트로젠제의 작용기전)

  • Lee, Jung-Bin;Yoon, Mi-Chung;Kim, Chang-Mee;Hong, Sa-Suk;Ryu, Kyung-Za
    • The Korean Journal of Pharmacology
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    • v.26 no.2
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    • pp.167-176
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    • 1990
  • In the present study, we examined the effects of tamoxifen and LY117018 on various parameters for the estrogenic actions in order to understand the mechanism by which tamoxifen and LY117018 act on the uterine cells in 21-23 day old immature rats. Tamoxifen and LY117018 stimulated uterine weight and uterine contents of DNA, protein, and peroxidase activity in the absence of estradiol while inhibited above parameters in the presence of estradiol. Both cytosolic and nuclear progesterone receptors were increased by the treatment of tamoxifen and LY117018 as well as estradiol, but estradiol-induced increase in the progesterone receptors were reduced by the treatment of antiestrogens. These effects were enhanced by the multiple injections of antiestrogens. It seemed that tamoxifen was more agonistic than LY117018 but less antagonistic than LY117018, judged by their effects on various parameters for the estrogenic action. The affinities of estradiol, tamoxifen, and LY117018 for the estrogen receptor were $0.17{\pm}0.01nM(100%)$, $1.10{\pm}0.01nM(6.3%)$, and $0.23{\pm}0.01nM(77%)$, respectively. Furthermore, LY117018 was the competitive ligand for the estrogen receptor in dose-related manner but tamoxifen was not. Following estradiol treatment, nuclear estrogen receptor was sharply increased by 1 h, reaching the maximum by 16 h, while tamoxifen and LY117018 slightly increased nuclear estrogen receptor by 1 h and then decreased thereafter. It is therefore concluded that LY117018 is a competitive antagonist for the estrogen receptor with less estrogenic activity, compared to tamoxifen with low affinity to the estrogen receptor, and tamoxifen may act through other binding site than the estrogen receptor.

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Steroid Hormone Receptor/Reporter Gene Transcription Assay for Food Additives and Contaminants

  • Jeong Sang-Hee;Cho Joon-Hyoung;Park Jong-Myung
    • Toxicological Research
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    • v.22 no.1
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    • pp.15-22
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    • 2006
  • Many of endocrine disrupting chemicals induce effects via interaction with hormone receptors and responsive elements in target cells. We investigated endocrine disrupting effects of some food additives and contaminants including BHA, BHT, ethoxyquin, propionic acid, sorbic acid, benzoic acid, CPM, aflatoxin B1, cadmium chloride, genistein, TCDD and PCBs in yeast transformants expressing human steroid hormone receptors along with steroid responsive elements. The response limit of genetically recombinant yeast to $17{\beta}$-estradiol, testosterone and progesterone was $1{\times}10^{-16},\;1{\times}10^{-12}\;and\;1{\times}10^{-13}M$, respectively. BHT induced weak transcriptional activity in estrogen sensitive yeast, while BHA and sorbic acid interacted weakly with androgen receptor/responsive element. CPM induced transcriptional activities in all types of yeasts sensitive to steroid hormones. Zearalenone and genistein induced high transcriptional activation in estrogen sensitive yeast with relative potencies almost $10^8$ folds lower than $17{\beta}$-estradiol. TCDD induced transcriptional activation weakly in estrogen- and progesterone- sensitive yeasts. This study elucidated that recombinant yeast is a sensitive and high-throughput system and can be used for the direct assessment on chemical interactions with steroid receptors and responsive elements. Also, the present study raises the requirement of evaluation on the endocrine disrupting effects of BHT, BHA, sorbic acid, CPM and TCDD for their transcription activity in yeast screening system though weak in intensity.

Insulin Resistance in Late Pregnant Rats (임신 후반기 흰쥐의 인슐린 저항성과 그 기전)

  • Chun, Myung-Heup;Kim, Yong-Woon;Park, So-Young;Kim, Jong-Yeon;Lee, Suck-Kang
    • Journal of Yeungnam Medical Science
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    • v.12 no.2
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    • pp.319-330
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    • 1995
  • The influence of normal late pregnancy on insulin action and insulin secretion was studied in the Sprague-Dawley female rats. On 20th day after mating, intravenous glucose tolerance test(IVGTT) was performed in non pregnant control and pregnant rats. As results of IVGTT, glucose disappearance rate was not significantly different in both groups, but secretory response of insulin was significantly(p<0.05) increased in pregnant rat. And the ratio of insulin/glucose was significantly higher in pregnant rats, which means existence of insulin resistance. These insulin resistance was overcomed by increased secretory response of pancreatic insulin. Insulinogenic index(${\Delta}$ insulin/glucose - 5 min) was highly significantly (r=0.62, p<0.01) correlated with progesterone concentration. Glycogen level and amounts of $^{14}C$-glucose incorporated into glycogen after IVGTT were significantly(p<0.05) decreased in the liver, but were not changed significantly in soleus. Glycogen synthase activity of soleus and liver was not differ significantly in the both groups. Insulin binding at varying concentrations of insulin to crude membrane of pregnant liver was not significantly different from control. In conclusions, although these pregnant rats were normal glucose tolerance due to increased secretory response of insulin, that was correlated with progesterone concentration, pregnant rat had insulin resistance. The mechanisms of insulin resistance were not related to defect of insulin binding phase and glycogen synthase, but suggest pre-receptor and/or postreceptor phase.

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Roles of Local Estrogen and Progesterone Mediated Receptors in the Regulation of Endometrial Inflammation (자궁내막 염증에 대한 지엽적 에스트로겐 및 프로게스테론 매개 수용체의 역할)

  • Gyesik Min
    • Journal of Life Science
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    • v.33 no.1
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    • pp.102-113
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    • 2023
  • This review discusses the cellular and molecular mechanisms by which the endometrial estrogen and progesterone receptors regulate local estrogen production, expression of the specific estrogen receptors, progesterone resistance, inflammatory responses and the differentiation and survival of endometriotic cells in endometrial inflammation. The epigenetic aberrations of endometrial stromal cells play an important role in the pathogenesis and progression of endometriosis. In particular, differential methylation of the estrogen receptor genes changes in the stromal cells the dominancy of estrogen receptor from ERα into ERβ, and results in the abnormal estrogen responses including inflammation, progesterone resistance and the disturbance of retinoid synthesis. These stromal cells also stimulate local estrogen production in response to PGE2 and the SF-1 mediated induction of steroidogenic enzyme expression, and the increased estradiol then feeds back into the ERβ to repeat the vicious inflammatory cycle through the activation of COX-2. In addition, high levels of ERβ expression may also change the chromatin structure of endometrial mesenchymal stem cells, and together with the repeated menstrual cycles can induce formation of the endometriotic tissue. The cascade of these serial events then leads to cell adhesion, angiogenesis and survival of the differentiation-disregulated stromal cells through the action of inflammatory factors such as ERβ-mediated estrogen, TNF-α and TGF-β1. Therefore, understanding of the dynamic hormonal changes during the menstrual cycle and the corresponding signal transduction mechanisms of the related nuclear receptors in endometrium would provide new insights for treating inflammatory diseases such as the endometriosis.

Regulation of Laminin Chain Gene Expression by Ovaria Steroid Hormones in Uterine Tissues of Ovariectomized Mice

  • Chanseob Shim;Dongho Geum;Park, Donchan
    • Animal cells and systems
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    • v.1 no.1
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    • pp.115-121
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    • 1997
  • To precisely analyze the role of ovarian steroids in the regulation of laminin chain gene expression in mouse uterine tissues, the ovariectomized mouse model was used. Ovariectomized mice received a single injection of steroid hormones and total RNA was isolated from whole uterine tissues. Messenger RNA levels of each laminin chain (A, 81, and 82) were determined by competitive RT-peR procedures. Estradiol decreased mRNA levels of laminin 81 chain about two-fold, and 82 chain rather moderately. Estradiol-induced inhibition of laminin 81 and 82 chain mRNA levels were completely blocked by pretreatment with estrogen receptor antagonist tamoxifen. Estriol, a short acting estrogen which cannot induce hyperplastic responses of rodent uterine tissues, also showed an inhibitory effect on 81 and 82 chain mRNA levels, while estrone, an inactive estrogen, failed to influence either 8 chain mRNA levels. Effects of steroids on A chain mRNA level were quite different from those on 8 chains. Laminin A chain mRNA level was slightly increased by estradiol treatment, but negatively affected by progesterone. Progesterone treatment greatly increased both 8 chain mRNA levels, but slightly decreased A chain mRNA level compared to the control. The effect of progesterone on laminin chain-specific mRNA levels was further increased by co-injection of estradiol in a time-dependent manner. Progesterone-induced 81 and 82 chain mRNA transcription was inhibited by RU486, a synthetic anti-progesterone /anti-glucocorticoid. The present study demonstrates for the first time that steroids are able to regulate laminin gene expression in mouse uterine tissues, indicating that steroid-regulated laminin gene expression is involved in uterine growth and probably differentiation.

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