scholarly journals Rat Uterine Oxytocin Receptor and Estrogen Receptor α and β mRNA Levels are Regulated by Estrogen Through Multiple Estrogen Receptors

2014 ◽  
Vol 60 (1) ◽  
pp. 55-61 ◽  
Author(s):  
Takuya MURATA ◽  
Kazumi NARITA ◽  
Toru ICHIMARU
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptors ◽  
Estrogen Receptor Α ◽  
Oxytocin Receptor ◽  
Mrna Levels

scholarly journals Inhibition of Oxytocin Receptor and Estrogen Receptor-α Expression, But Not Relaxin Receptors (LGR7), in the Myometrium of Late Pregnant Relaxin Gene Knockout Mice

Endocrinology ◽  
2003 ◽  
Vol 144 (10) ◽  
pp. 4272-4275 ◽  
Author(s):  
Andrew L. Siebel ◽  
Helen M. Gehring ◽  
Irna Grace T. Reytomas ◽  
Laura J. Parry
Keyword(s):  
Gene Expression ◽  
Estrogen Receptor ◽  
Knockout Mice ◽  
Gene Knockout ◽  
Estrogen Receptor Α ◽  
Oxytocin Receptor ◽  
Receptor Expression ◽  
Late Gestation ◽  
Mrna Levels ◽  
Gene Knockout Mice

This study used relaxin (RLX) gene knockout mice (Rlx−/−) to investigate the effects of RLX on myometrial oxytocin receptor (OTR) and estrogen receptor (ER)-α gene expression in late gestation. We also characterized the temporal expression of the RLX receptor (LGR7) and demonstrated gene transcripts in the myometrium of Rlx+/+ and Rlx−/− mice. There was a significant (P < 0.05) decrease in myometrial LGR7 gene expression on d 17.5 and 18.5 post coitum (pc) compared with earlier stages of gestation, but no differences between Rlx+/+ and Rlx−/− mice. Myometrial OTR mRNA levels increased at the end of gestation in Rlx+/+ but not Rlx−/− mice. ERα gene expression was up-regulated on d 14.5 pc in Rlx+/+ mice, with mRNA levels remaining high throughout late gestation. In contrast, ERα mRNA levels were significantly lower in Rlx−/− mice on d 14.5 and 18.5 pc. These data show that the increases in myometrial OTR and ERα expression in late pregnant Rlx+/+ mice were attenuated in Rlx−/− mice. The effects of RLX on OTRs are probably mediated via activation of ERα. Finally, RLX receptor expression in the myometrium of Rlx−/− mice did not differ from wild-type mice, implying that RLX does not influence expression of its receptor.

scholarly journals Differential Expression of Myometrial Oxytocin Receptor and Prostaglandin H Synthase 2, But Not Estrogen Receptor α and Heat Shock Protein 90 Messenger Ribonucleic Acid in the Gravid Horn and Nongravid Horn in Sheep during Betamethasone-Induced Labor1

Endocrinology ◽  
1999 ◽  
Vol 140 (12) ◽  
pp. 5712-5718 ◽  
Author(s):  
Wen Xuan Wu ◽  
Xiao Hong Ma ◽  
Toshiyuki Yoshizato ◽  
Norio Shinozuka ◽  
Peter W. Nathanielsz
Keyword(s):  
Estrogen Receptor ◽  
Mrna Expression ◽  
Heat Shock Protein 90 ◽  
Late Pregnancy ◽  
Mechanical Stretch ◽  
Estrogen Receptor Α ◽  
Oxytocin Receptor ◽  
Induced Labor ◽  
Prostaglandin H ◽  
Term Labor

Abstract In the present study, we characterized four myometrial contraction-associated proteins (mCAPs): oxytocin receptor (OTR), prostaglandin H synthase 2 (PGHS2), estrogen receptor α (ERα), and heat shock protein 90 (Hsp90) messenger RNA (mRNA) expression in the nongravid horn of pregnant sheep and compared them with their expression in the gravid horn that is exposed to a greater degree of stretch. We also examined the regulatory effects of estrogen and progesterone on OTR mRNA expression in ovariectomized nonpregnant sheep. In addition, we determined the ontogeny of mCAP expression in the gravid horn throughout late pregnancy and during spontaneous term labor. Gravid horn and nongravid horn myometria were removed under general anesthesia from control ewes not in labor at 130–140 days gestational age (dGA; n = 3) and during betamethasone-induced labor (n = 6) at the same gestational age. Gravid horn myometrium was also collected from ewes not in labor at 95 dGA (n = 3), 101–110 dGA (n = 3), 111–120 dGA (n = 3), 121–130 dGA (n = 3), 131–140 dGA (n = 3), and 141–145 dGA (n = 4) and from ewes in spontaneous term labor (n = 4). All ewes were carrying single fetuses. Myometrium was also collected from ovariectomized nonpregnant ewes treated with saline (n = 5), estradiol (50 μg/day; n = 5), progesterone (0.3 g, intravaginally; n = 5), and estradiol plus progesterone (n = 5). Myometrial RNA was extracted and analyzed by Northern blot for OTR, PGHS2, ERα, and Hsp90 mRNA, normalized for 18S ribosomal RNA orβ -actin. ERα, Hsp90, OTR, and PGHS2 mRNA were all significantly up-regulated during betamethasone-induced labor (P< 0.01) in gravid and nongravid horn myometrium. The level of gravid horn OTR mRNA during labor was 3 times the level of nongravid horn OTR mRNA (P < 0.0001). Gravid horn PGHS2 mRNA was also higher than nongravid horn PGHS2 (P < 0.02). In contrast, in spontaneous term labor nongravid horn, ERα and Hsp90 mRNA were similar to gravid horn. Myometrial ERα and Hsp90 mRNA remained unchanged throughout late pregnancy and increased at spontaneous term labor (P < 0.05). In contrast, myometrial OTR increased around 130 dGA (P < 0.01) and further increased at spontaneous term labor (P< 0.02). Progesterone significantly inhibited myometrial OTR mRNA expression in nonpregnant sheep and estradiol antagonized progesterone’s inhibitory effect. Mechanical stretch differentially regulated mCAP mRNA expression in the ovine gravid horn and nongravid horn. Mechanical stretch appears largely responsible for increased OTR mRNA and to a lesser degree PGHS2 mRNA. In addition, endocrine factors may be required for full activation of OTR and PGHS2 mRNA associated with labor. ERα and Hsp90 mRNA are not under the control of uterine stretch in keeping with our previous results, indicating that systemic hormones such as estradiol, are prime regulators for these two mCAP mRNA expression during labor.

Alteration in Estrogen Receptor α mRNA Levels in Frontal Cortex and Hippocampus of Patients with Major Mental Illness

2005 ◽  
Vol 58 (10) ◽  
pp. 812-824 ◽  
Author(s):  
William R. Perlman ◽  
Eva Tomaskovic-Crook ◽  
Deidra M. Montague ◽  
Maree J. Webster ◽  
David R. Rubinow ◽  
...  
Keyword(s):  
Mental Illness ◽  
Estrogen Receptor ◽  
Frontal Cortex ◽  
Estrogen Receptor Α ◽  
Mrna Levels

scholarly journals Sexually Dimorphic Effect of Genistein on Hypothalamic Neuronal Differentiation in Vitro

2019 ◽  
Vol 20 (10) ◽  
pp. 2465 ◽  
Author(s):  
Marilena Marraudino ◽  
Alice Farinetti ◽  
Maria-Angeles Arevalo ◽  
Stefano Gotti ◽  
GianCarlo Panzica ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Sex Differences ◽  
Estrogen Receptors ◽  
Estrogen Receptor Α ◽  
Neuronal Cultures ◽  
Sexually Dimorphic ◽  
Hypothalamic Neurons ◽  
Estrogen Receptor Antagonists

Developmental actions of estradiol in the hypothalamus are well characterized. This hormone generates sex differences in the development of hypothalamic neuronal circuits controlling neuroendocrine events, feeding, growth, reproduction and behavior. In vitro, estradiol promotes sexually dimorphic effects on hypothalamic neuritogenesis. Previous studies have shown that developmental actions of the phytoestrogen genistein result in permanent sexually dimorphic effects in some behaviors and neural circuits in vivo. In the present study, we have explored if genistein, like estradiol, affects neuritogenesis in primary hypothalamic neurons and investigated the estrogen receptors implicated in this action. Hypothalamic neuronal cultures, obtained from male or female embryonic day 14 (E14) CD1 mice, were treated with genistein (0.1 µM, 0.5 µM or 1 µM) or vehicle. Under basal conditions, female neurons had longer primary neurites, higher number of secondary neurites and higher neuritic arborization compared to male neurons. The treatment with genistein increased neuritic arborization and the number of primary neurites and decreased the number of secondary neurites in female neurons, but not in male neurons. In contrast, genistein resulted in a significant increase in primary neuritic length in male neurons, but not in female neurons. The use of selective estrogen receptor antagonists suggests that estrogen receptor α, estrogen receptor β and G-protein-coupled estrogen receptors are involved in the neuritogenic action of genistein. In summary, these findings indicate that genistein exerts sexually dimorphic actions on the development of hypothalamic neurons, altering the normal pattern of sex differences in neuritogenesis.

scholarly journals Estrogen Receptor (ER)-β Reduces ERα-Regulated Gene Transcription, Supporting a “Ying Yang” Relationship between ERα and ERβ in Mice

2003 ◽  
Vol 17 (2) ◽  
pp. 203-208 ◽  
Author(s):  
Marie K. Lindberg ◽  
Sofia Movérare ◽  
Stanko Skrtic ◽  
Hui Gao ◽  
Karin Dahlman-Wright ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Gene Transcription ◽  
Physiological Role ◽  
Estrogen Receptor Α ◽  
Mrna Levels ◽  
Wild Type ◽  
Ovariectomized Mice ◽  
Adult Bone

Abstract Estrogen is of importance for the regulation of adult bone metabolism. The aim of the present study was to determine the role of estrogen receptor-β (ERβ) in vivo on global estrogen-regulated transcriptional activity in bone. The effect of estrogen in bone of ovariectomized mice was determined using microarray analysis including 9400 genes. Most of the genes (95% = 240 genes) that were increased by estrogen in wild-type (WT) mice were also increased by estrogen in ERβ-inactivated mice. Interestingly, the average stimulatory effect of estrogen on the mRNA levels of these genes was 85% higher in ERβ-inactivated than in WT mice, demonstrating that ERβ reduces estrogen receptor-α (ERα)-regulated gene transcription in bone. The average stimulatory effect of estrogen on estrogen-regulated bone genes in ERα-inactivated mice was intermediate between that seen in WT and ERαβ double-inactivated mice. Thus, ERβ inhibits ERα-mediated gene transcription in the presence of ERα, whereas, in the absence of ERα, it can partially replace ERα. In conclusion, our in vivo data indicate that an important physiological role of ERβ is to modulate ERα-mediated gene transcription supporting a “Ying Yang” relationship between ERα and ERβ in mice.

scholarly journals Estrogen receptor-β regulates mechanical signaling in primary osteoblasts

2014 ◽  
Vol 306 (8) ◽  
pp. E937-E944 ◽  
Author(s):  
Alesha B. Castillo ◽  
Jason W. Triplett ◽  
Fredrick M. Pavalko ◽  
Charles H. Turner
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptors ◽  
Fluid Shear Stress ◽  
Nuclear Translocation ◽  
Estrogen Receptor Α ◽  
Bone Adaptation ◽  
Mitogen Activated Protein Kinase ◽  
Prostaglandin E ◽  
Mechanical Signaling ◽  
Age Related

Mechanical loading is an important regulator in skeletal growth, maintenance, and aging. Estrogen receptors have a regulatory role in mechanically induced bone adaptation. Estrogen receptor-α (ERα) is known to enhance load-induced bone formation, whereas ERβ negatively regulates this process. We hypothesized that ERβ regulates mechanical signaling in osteoblasts. We tested this hypothesis by subjecting primary calvarial cells isolated from wild-type and ERβ-knockout mice (BERKO) to oscillatory fluid flow in the absence or presence of estradiol (E2). We found that the known responses to fluid shear stress, i.e., phosphorylation of the mitogen-activated protein kinase ERK and upregulation of COX-2 expression, were inhibited in BERKO cells in the absence of E2. Flow-induced increase in prostaglandin E2 (PGE2) release was not altered in BERKO cells in the absence of E2, but was increased when E2 was present. Additionally, immunofluorescence analysis and estrogen response element luciferase assays revealed increased ERα expression and flow- and ligand-induced nuclear translocation as well as transcriptional activity in BERKO cells in both the presence and absence of E2. Taken together, these data suggest that ERβ plays both ligand-dependent and ligand-independent roles in mechanical signaling in osteoblasts. Furthermore, our data suggest that one mechanism by which ERβ regulates mechanotransduction in osteoblasts may result from its inhibitory effect on ERα expression and function. Targeting estrogen receptors (e.g., inhibiting ERβ) may represent an effective approach for prevention and treatment of age-related bone loss.

scholarly journals Expression of Estrogen Receptor α and β in the Rhesus Monkey Corpus Luteum during the Menstrual Cycle: Regulation by Luteinizing Hormone and Progesterone*

Endocrinology ◽  
2000 ◽  
Vol 141 (5) ◽  
pp. 1711-1717 ◽  
Author(s):  
Diane M. Duffy ◽  
Charles L. Chaffin ◽  
Richard L. Stouffer
Keyword(s):  
Estrogen Receptor ◽  
Menstrual Cycle ◽  
Corpus Luteum ◽  
Messenger Rna ◽  
Luteal Phase ◽  
Estrogen Receptor Α ◽  
Corpora Lutea ◽  
Mrna Levels ◽  
Protein Levels ◽  
Late Luteal Phase

Abstract There are conflicting reports on the presence or absence of estrogen receptor (ER) in the primate corpus luteum, and the discovery of a second type of estrogen receptor, ERβ, adds an additional level of complexity. To reevaluate ER expression in the primate luteal tissue, we used semiquantitative RT-PCR based assays and Western blotting to assess ERα and β messenger RNA (mRNA) and protein levels in corpora lutea (n = 3/stage) obtained from adult female rhesus monkeys at early (days 3–5), mid (days 6–8), mid-late (days 10–12), and late (days 14–16) luteal phase of the natural menstrual cycle. ERα mRNA levels did not vary across the stages of the luteal phase, and ERα protein was not consistently detected in luteal tissues. However, ERβ mRNA and protein levels were detectable in early and mid luteal phases and increased (P < 0.05) to peak levels at mid-late luteal phase before declining by late luteal phase. To determine if ERβ mRNA expression in the corpus luteum is regulated by LH, monkeys received the GnRH antagonist antide either alone or with 3 daily injections of LH to simulate pulsatile LH release. Treatment with antide alone or concomitant LH administration did not alter luteal ERβ mRNA levels. When monkeys also received the 3β-hydroxysteroid dehydrogenase inhibitor trilostane to reduce luteal progesterone production, luteal ERβ mRNA levels were 3-fold higher (P < 0.05) than in monkeys receiving antide + LH only. Replacement of progestin activity with R5020 reduced luteal ERβ mRNA levels to those seen in animals receiving antide + LH. Thus, there is dynamic ERβ expression in the primate corpus luteum during the menstrual cycle, consistent with a role for estrogen in the regulation of primate luteal function and life span via a receptor (ERβ)-mediated pathway. Increased ERβ expression in the progestin-depleted corpus luteum during LH exposure suggests that the relative progestin deprivation experienced by the corpus luteum between LH pulses may enhance luteal sensitivity to estrogens during the late luteal phase of the menstrual cycle.

scholarly journals The Role of Estrogen Receptors in Urothelial Cancer

2021 ◽  
Vol 12 ◽  
Author(s):  
Takuro Goto ◽  
Hiroshi Miyamoto
Keyword(s):  
Bladder Cancer ◽  
Estrogen Receptor ◽  
Estrogen Receptors ◽  
Cancer Progression ◽  
Urothelial Cancer ◽  
Epidemiological Data ◽  
Estrogen Receptor Α ◽  
Estrogen Receptor Signaling ◽  
Stage Disease ◽  
Immunohistochemical Studies

Epidemiological data have indicated that there are some sex-related differences in bladder cancer. Indeed, the incidence of bladder cancer in men has been substantially higher than that in women throughout the world, while women tend to have higher stage disease and poorer prognosis. These gender disparities have prompted to investigate sex hormones and their cognitive receptors in bladder cancer. Specifically, estrogen receptors, including estrogen receptor-α and estrogen receptor-β, have been shown to contribute to urothelial carcinogenesis and cancer progression, as well as to modulating chemosensitivity in bladder cancer, although conflicting findings exist. Meanwhile, immunohistochemical studies in surgical specimens have assessed the expression of estrogen receptors and related proteins as well as its associations with clinicopathologic features of bladder cancer and patient outcomes. This review article summarizes and discusses available data indicating that estrogen receptor signaling plays an important role in urothelial cancer.

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