scholarly journals ERα-dependent stimulation of LCN2 in uterine epithelium during mouse early pregnancy

Reproduction ◽  
2020 ◽  
Vol 159 (4) ◽  
pp. 493-501
Author(s):  
Y-F Liu ◽  
M-Y Li ◽  
Y-P Yan ◽  
W Wei ◽  
B Li ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Estrogen Receptor ◽  
Bacterial Infection ◽  
Early Pregnancy ◽  
Estrogen Receptor Α ◽  
Bacterial Activity ◽  
Uterine Epithelium ◽  
Estrogen Treatment ◽  
Lipocalin 2 ◽  
Estrogen Regulation

Maintenance of a suitable uterine milieu is important for embryo development and subsequent implantation during early pregnancy. High estrogen level in proestrous and estrous stages is essential for uterine anti-bacterial activity during preimplantation period. Lipocalin-2 is an essential molecule which prevents bacterial infection by sequestering iron. In this study, the highest expression of lipocalin-2 is observed in the endometrial epithelium on day 1 of normal pregnancy and pseudopregnancy, which exhibit a similar hormone scenario. By injecting the agonists for estrogen receptor α and estrogen receptor β in ovariectomized mice, we found estrogen receptor α is the dominant member for estrogen regulation on lipocalin-2 expression. Estrogen treatment in estrogen receptor α-knockout mice further confirmed the role of estrogen receptor α. Using published data from whole-genome estrogen receptor α binding site assay, significant estrogen receptor α recruitment peaks are found at the downstream of lipocalin-2 gene after estrogen treatment. Furthermore, to study the anti-bacterial activity of lipocalin-2 in uterus, Escherichia coli is injected to mimic bacterial infection. Our results showed an obvious induction of lipocalin-2 in Escherichia coli-treated group. Taken together, this study indicates estrogen regulation of lipocalin-2 in uterine epithelium is mediated by estrogen receptor α, and lipocalin-2 may have anti-bacterial activity during early pregnancy.

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 Klotho/fibroblast growth factor 23- and PTH-independent estrogen receptor-α-mediated direct downregulation of NaPi-IIa by estrogen in the mouse kidney

2016 ◽  
Vol 311 (2) ◽  
pp. F249-F259 ◽  
Author(s):  
Rose Webster ◽  
Sulaiman Sheriff ◽  
Rashma Faroqui ◽  
Faraaz Siddiqui ◽  
John R. Hawse ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Growth Factor ◽  
Food Intake ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Estrogen Receptor Α ◽  
Estrogen Treatment ◽  
Fibroblast Growth ◽  
Reading Frame ◽  
Receptor Isoforms

Estrogen treatment causes renal phosphate (Pi) wasting and hypophosphatemia in rats and humans; however, the signaling mechanisms mediating this effect are still poorly understood. To determine the specific roles of estrogen receptor isoforms (ERα and ERβ) and the Klotho pathway in mediating these effects, we studied the effects of estrogen on renal Pi handling in female mice with null mutations of ERα or ERβ or Klotho and their wild type (WT) using balance studies in metabolic cages. Estrogen treatment of WT and ERβ knockout (KO) mice caused a significant reduction in food intake along with increased renal phosphate wasting. The latter resulted from a significant downregulation of NaPi-IIa and NaPi-IIc protein abundance. The mRNA expression levels of both transporters were unchanged in estrogen-treated mice. These effects on both food intake and renal Pi handling were absent in ERα KO mice. Estrogen treatment of Klotho KO mice or parathyroid hormone (PTH)-depleted thyroparathyroidectomized mice exhibited a significant downregulation of NaPi-IIa with no change in the abundance of NaPi-IIc. Estrogen treatment of a cell line (U20S) stably coexpressing both ERα and ERβ caused a significant downregulation of NaPi-IIa protein when transiently transfected with a plasmid containing full-length or open-reading frame (ORF) 3′-untranslated region (UTR) but not 5′-UTR ORF of mouse NaPi-IIa transcript. In conclusion, estrogen causes phosphaturia and hypophosphatemia in mice. These effects result from downregulation of NaPi-IIa and NaPi-IIc proteins in the proximal tubule through the activation of ERα. The downregulation of NaPi-IIa by estrogen involves 3′-UTR of its mRNA and is independent of Klotho/fibroblast growth factor 23 and PTH signaling pathways.

Structure, tissue distribution and estrogen regulation of splice variants of the sea bream estrogen receptor α gene

Gene ◽  
2012 ◽  
Vol 503 (1) ◽  
pp. 18-24 ◽  
Author(s):  
P.I.S. Pinto ◽  
R. Teodósio ◽  
S. Socorro ◽  
D.M. Power ◽  
A.V.M. Canário
Keyword(s):  
Estrogen Receptor ◽  
Tissue Distribution ◽  
Splice Variants ◽  
Estrogen Receptor Α ◽  
Sea Bream ◽  
Estrogen Regulation ◽  
Estrogen Receptor Α Gene

Estrogen regulation of trefoil factor 1 expression by estrogen receptor α and Sp proteins

2005 ◽  
Vol 302 (1) ◽  
pp. 96-107 ◽  
Author(s):  
Jian-Min Sun ◽  
Virginia A. Spencer ◽  
Lin Li ◽  
Hou Yu Chen ◽  
Jenny Yu ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Α ◽  
Trefoil Factor ◽  
Estrogen Regulation ◽  
Trefoil Factor 1

scholarly journals Genomic Priming of the Antisecretory Response to Estrogen in Rat Distal Colon throughout the Estrous Cycle

2009 ◽  
Vol 30 (6) ◽  
pp. 751-751
Author(s):  
Fiona O'Mahony ◽  
Rodrigo Alzamora ◽  
Ho-Lam Chung ◽  
Warren Thomas ◽  
Brian J. Harvey
Keyword(s):  
Estrogen Receptor ◽  
Estrous Cycle ◽  
Intestinal Secretion ◽  
Distal Colon ◽  
Estrogen Receptor Α ◽  
Transcriptional Level ◽  
Colonic Crypt ◽  
Estrogen Regulation ◽  
Antisecretory Effect ◽  
Crypt Cells

ABSTRACT The secretion of Cl− across distal colonic crypt cells provides the driving force for the movement of fluid into the luminal space. 17β-Estradiol (E2) produces a rapid and sustained reduction in secretion in females, which is dependent on the novel protein kinase Cδ (PKCδ) isozyme and PKA isoform I targeting of KCNQ1 channels. This sexual dimorphism in the E2 response is associated with a higher expression level of PKCδ in female compared with the male tissue. The present study revealed the antisecretory response is regulated throughout the female reproductive (estrous) cycle and is primed by genomic regulation of the kinases. E2 (1-10 nm) decreased cAMP-dependent secretion in colonic epithelia during the estrous, metestrous, and diestrous stages. A weak inhibition of secretion was demonstrated in the proestrous stage. The expression levels of PKCδ and PKA fluctuated throughout the estrous cycle and correlated with the potency of the antisecretory effect of E2. The expression of PKCδ and PKA were up-regulated by estrogen at a transcriptional level via a PKCδ-MAPK-cAMP response element-binding protein-regulated pathway indicating a genomic priming of the antisecretory response. PKCδ was activated by the membrane-impermeant E2-BSA, and this response was inhibited by the estrogen receptor antagonist ICI 182,780. The 66-kDa estrogen receptor-α isoform was present at the plasma membrane of female colonic crypt cells with a lower abundance found in male colonic crypts. The study demonstrates estrogen regulation of intestinal secretion both at a rapid and transcriptional level, demonstrating an interdependent relationship between both nongenomic and genomic hormone responses.

scholarly journals Glucocorticoid Inhibition of Estrogen Regulation of the Serotonin Receptor 2B in Cardiomyocytes Exacerbates Cell Death in Hypoxia/Reoxygenation Injury

2021 ◽  
Author(s):  
Hemangini A. Dhaibar ◽  
Natalie G. Carroll ◽  
Shripa Amatya ◽  
Lilly Kamberov ◽  
Pranshu Khanna ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Estrogen Receptor ◽  
Glucocorticoid Receptor ◽  
Serotonin Receptor ◽  
Estrogen Receptor Α ◽  
Estrogen Regulation ◽  
Reoxygenation Injury ◽  
Effects Of Stress ◽  
Serotonin Receptor 2B ◽  
Hypoxia Reoxygenation

Background Stress has emerged as an important risk factor for heart disease in women. Stress levels have been shown to correlate with delayed recovery and increased mortality after a myocardial infarction. Therefore, we sought to investigate if the observed sex‐specific effects of stress in myocardial infarction may be partly attributed to genomic interactions between the female sex hormones, estrogen (E2), and the primary stress hormones glucocorticoids. Methods and Results Genomewide studies show that glucocorticoids inhibit estrogen‐mediated regulation of genes with established roles in cardiomyocyte homeostasis. These include 5‐HT2BR (cardiac serotonin receptor 2B), the expression of which is critical to prevent cardiomyocyte death in the adult heart. Using siRNA, gene expression, and chromatin immunoprecipitation assays, we found that 5‐HT2BR is a primary target of the glucocorticoid receptor and the estrogen receptor α at the level of transcription. The glucocorticoid receptor blocks the recruitment of estrogen receptor α to the promoter of the 5‐HT2BR gene, which may contribute to the adverse effects of stress in the heart of premenopausal women. Using immunoblotting, TUNEL (terminal deoxynucleotidal transferase–mediated biotin–deoxyuridine triphosphate nick‐end labeling), and flow cytometry, we demonstrate that estrogen decreases cardiomyocyte death by a mechanism relying on 5‐HT2BR expression. In vitro and in vivo experiments show that glucocorticoids inhibit estrogen cardioprotection in response to hypoxia/reoxygenation injury and exacerbate the size of the infarct areas in myocardial infarction. Conclusions These results established a novel mechanism underlying the deleterious effects of stress on female cardiac health in the setting of ischemia/reperfusion.

scholarly journals Reproductive Senescence Blunts Response of Estrogen Receptor-α Expression to Estrogen Treatment in Rat Post-Ischemic Cerebral Microvessels

PLoS ONE ◽  
2014 ◽  
Vol 9 (7) ◽  
pp. e102194 ◽  
Author(s):  
Emil Zeynalov ◽  
Niloofar Rezvani ◽  
Chikao Miyazaki ◽  
Xiaoguang Liu ◽  
Marguerite T. Littleton-Kearney
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Α ◽  
Estrogen Treatment ◽  
Cerebral Microvessels ◽  
Reproductive Senescence

Estrogen regulation of the transient outward K+ current involves estrogen receptor α in mouse heart

2015 ◽  
Vol 86 ◽  
pp. 85-94 ◽  
Author(s):  
Gracia El Gebeily ◽  
Nabil El Khoury ◽  
Sophie Mathieu ◽  
Judith Brouillette ◽  
Céline Fiset
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Α ◽  
Mouse Heart ◽  
Estrogen Regulation ◽  
K Current
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