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.

G-protein Coupled Estrogen Receptor Expression in Growth Hormone Secreting and Non-Functioning Adenomas

2020 ◽  
Author(s):  
Hande Mefkure Ozkaya ◽  
Muge Sayitoglu ◽  
Nil Comunoglu ◽  
Eda Sun ◽  
Fatma Ela Keskin ◽  
...  
Keyword(s):  
Gene Expression ◽  
Estrogen Receptor ◽  
Protein Expression ◽  
G Protein ◽  
Estrogen Receptor Α ◽  
Receptor Expression ◽  
Positive Correlation ◽  
Polymerase Chain ◽  
G Protein Coupled ◽  
Transforming Gene

Abstract Purpose To evaluate the expression of G-protein coupled estrogen receptor (GPER1), aromatase, estrogen receptor α (ERα), estrogen receptor β (ERβ), pituitary tumor transforming gene (PTTG), and fibroblast growth factor 2 (FGF2) in GH-secreting and non-functioning adenomas (NFA). Methods Thirty patients with acromegaly and 27 patients with NFA were included. Gene expression was determined via quantitative reverse transcription polymerase chain reaction (QRT-PCR). Protein expression was determined via immunohistochemistry. Results There was no difference, in terms of gene expression of aromatase, ERα, PTTG, and FGF2 between the two groups (p>0.05 for all). ERβ gene expression was higher and GPER1 gene expression was lower in GH-secreting adenomas than NFAs (p<0.05 for all). Aromatase and ERβ protein expression was higher in GH-secreting adenomas than NFAs (p=0.01). None of the tumors expressed ERα. GPER1 expression was detected in 62.2% of the GH-secreting adenomas and 45% of NFAs. There was no difference in terms of GPER1, PTTG, FGF2 H scores between the two groups (p>0.05 for all). GPER1 gene expression was positively correlated to ERα, ERβ, PTTG, and FGF2 gene expression (p<0.05 for all). There was a positive correlation between aromatase and GPER1 protein expression (r=0.31; p=0.04). Conclusions GPER1 is expressed at both gene and protein level in a substantial portion of GH-secreting adenomas and NFAs. The finding of a positive correlation between GPER1 and ERα, ERβ, PTTG, and FGF2 gene expression and aromatase and GPER1 protein expression suggests GPER1 along with aromatase and classical ERs might mediate the effects of estrogen through upregulation of PTTG and FGF2.

scholarly journals Estrogen Regulation of Neurokinin B Gene Expression in the Mouse Arcuate Nucleus Is Mediated by Estrogen Receptor α

Endocrinology ◽  
2004 ◽  
Vol 145 (2) ◽  
pp. 736-742 ◽  
Author(s):  
Tammy L. Dellovade ◽  
Istvan Merchenthaler
Keyword(s):  
Gene Expression ◽  
Estrogen Receptor ◽  
Postmenopausal Women ◽  
Knockout Mice ◽  
Arcuate Nucleus ◽  
Estrogen Receptor Α ◽  
Estrogen Treatment ◽  
Ovariectomized Rats ◽  
Neurokinin B ◽  
Estrogen Regulation

Abstract Neurokinin B (NKB) gene expression is elevated in the infundibular (arcuate) nucleus of the hypothalamus in postmenopausal women. Estrogen replacement decreases both the number of NKB mRNA-expressing neurons and the level of expression within individual cells. Similarly, NKB gene expression is elevated in ovariectomized rats and reduced after estrogen treatment. The actions of estrogen in the brain can be mediated via either estrogen receptor α (ERα) or estrogen receptor β (ERβ). In the rodent arcuate nucleus (ARC), more ERα- than ERβ-containing cells are present, suggesting that ERα might be directly responsible for estrogen regulation of NKB gene expression. However, an indirect effect via ERβ could not be ruled out. Here we used ERα knockout and ERβ knockout mice to identify the type of ER responsible for mediating estrogen action on NKB gene expression in the ARC. Using in situ hybridization histochemistry, we have found that estrogen treatment significantly reduced NKB gene expression in the ARC of ovariectomized ERβ knockout mice, but had no effect on NKB mRNA levels in ERα knockout mice. These data indicate that ERα mediates the increase in NKB gene expression associated with ovariectomy in rodents and might also be responsible for the increase in NKB in postmenopausal women.

scholarly journals Estrogen Receptor α Inhibits IL-1β Induction of Gene Expression in the Mouse Liver

Endocrinology ◽  
2002 ◽  
Vol 143 (7) ◽  
pp. 2559-2570 ◽  
Author(s):  
Mark J. Evans ◽  
Kehdih Lai ◽  
Lucinda J. Shaw ◽  
Douglas C. Harnish ◽  
Christopher C. Chadwick
Keyword(s):  
Gene Expression ◽  
Estrogen Receptor ◽  
Knockout Mice ◽  
Ethinyl Estradiol ◽  
Binding Protein ◽  
Gene Induction ◽  
Estrogen Receptor Α ◽  
Ovariectomized Mice ◽  
Prostaglandin D Synthase ◽  
Short Heterodimer Partner

Abstract Estrogens have been suggested to modulate several inflammatory processes. Here, we show that IL-1β treatment induced the expression of approximately 75 genes in the liver of ovariectomized mice. 17α-Ethinyl estradiol (EE) pretreatment reduced the IL-1β induction of approximately one third of these genes. Estrogen receptor α (ERα) was required for this inhibitory activity, because EE inhibition of IL-1β-stimulated gene expression occurred in ERβ knockout mice, but not in ERα knockout mice. EE treatment induced expression of 40 genes, including the transcriptional repressor short heterodimer partner and prostaglandin D synthase, known modulators of nuclear factor-κB signaling. However, the ER agonists genistein and raloxifene both inhibited IL-1β gene induction without stimulating the expression of prostaglandin D synthase, short heterodimer partner, or other ER-inducible genes, indicating that induction of gene expression was not required for ER inhibition of IL-1β signaling. Finally, the ability of EE to repress IL-1β gene induction varied among tissues. For example, EE inhibited IL-1β induction of lipopolysaccharide-induced c-x-c chemokine (LIX) in the liver, but not in the spleen or lung. The degree of EE repression did not correlate with ER expression. cAMP response element binding protein-binding protein (CBP)/p300 levels also varied between tissues. Together, these results are consistent with a model of in vivo ER interference with IL-1β signaling through a coactivator-based mechanism.

scholarly journals Oxytocin Signal and Social Behaviour: Comparison among Adult and Infant Oxytocin, Oxytocin Receptor and CD38 Gene Knockout Mice

2010 ◽  
Vol 22 (5) ◽  
pp. 373-379 ◽  
Author(s):  
H. Higashida ◽  
O. Lopatina ◽  
T. Yoshihara ◽  
Y. A. Pichugina ◽  
A. A. Soumarokov ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Social Behaviour ◽  
Gene Knockout ◽  
Oxytocin Receptor ◽  
Gene Knockout Mice

scholarly journals Neonatal Exposure to Bisphenol A Alters Rat Uterine Implantation-Associated Gene Expression and Reduces the Number of Implantation Sites

Endocrinology ◽  
2011 ◽  
Vol 152 (3) ◽  
pp. 1101-1111 ◽  
Author(s):  
Jorgelina Varayoud ◽  
Jorge G. Ramos ◽  
Verónica L. Bosquiazzo ◽  
Melina Lower ◽  
Mónica Muñoz-de-Toro ◽  
...  
Keyword(s):  
Gene Expression ◽  
Estrogen Receptor ◽  
Bisphenol A ◽  
Steroid Receptors ◽  
Estrogen Receptor Α ◽  
Receptor Expression ◽  
Female Rats ◽  
Postnatal Exposure ◽  
Long Term Effects ◽  
Implantation Sites

Endocrine disrupters have been associated with reproductive pathologies such as infertility and gynecological tumors. Using a rat model of early postnatal exposure to bisphenol A (BPA), we evaluated the long-term effects on 1) female reproductive performance, 2) uterine homeobox A10 (Hoxa10) and Hoxa10-target gene expression, and 3) ovarian steroid levels and uterine estrogen receptor α and progesterone (P) receptor expression. Newborn female rats received vehicle, BPA.05 (0.05 mg/kg · d), BPA20 (20 mg/kg · d), diethylstilbestrol.2 (0.2 μg/kg · d), or diethylstilbestrol 20 (20 μg/kg · d) on postnatal d 1, 3, 5, and 7. A significant decrease in the number of implantation sites was assessed in the xenoestrogen-exposed females. To address the molecular effects of postnatal xenoestrogen exposure on the pregnant uterus, we evaluated the expression of implantation-associated genes on d 5 of pregnancy (preimplantation uterus). All xenoestrogen-treated rats showed a lower expression of Hoxa10. In the same animals, two Hoxa10-downstream genes were misregulated in the uterus. β3Integrin, which is up-regulated by Hoxa10 in controls, was decreased, whereas empty spiracles homolog 2, which is down-regulated by Hoxa10, was increased. Furthermore a clear down-regulation of estrogen receptor α and P receptor expression was detected without changes in estradiol and P serum levels. The early exposure to BPA produced a lower number of implantation sites in association with a defective uterine environment during the preimplantation period. Alterations in the endocrine-regulated Hoxa10 gene pathways (steroid receptors—Hoxa10—β3integrin/empty spiracles homolog 2) could explain, at least in part, the BPA effects on the implantation process.

scholarly journals Gene expression profiling of light-induced retinal degeneration in phototransduction gene knockout mice

2008 ◽  
Vol 40 (5) ◽  
pp. 495 ◽  
Author(s):  
Jayalakshmi Krishnan ◽  
Jiayan Chen ◽  
Kum-Joo Shin ◽  
Jong-Ik Hwang ◽  
Sang-Uk Han ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Expression Profiling ◽  
Retinal Degeneration ◽  
Knockout Mice ◽  
Expression Profiling ◽  
Gene Knockout ◽  
Gene Knockout Mice
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