Estrogen Receptor-Mediated Gene Transcription and Cistrome

2018 ◽  
pp. 49-70 ◽  
Author(s):  
Gregory Bick ◽  
Dan Zhao ◽  
Xiaoting Zhang
Keyword(s):  
Estrogen Receptor ◽  
Gene Transcription

scholarly journals Estrogen receptor-mediated repression of human hepatic lipase gene transcription

2002 ◽  
Vol 43 (3) ◽  
pp. 383-391 ◽  
Author(s):  
Daniel R. Jones ◽  
Robert J. Schmidt ◽  
Richard T. Pickard ◽  
Patricia S. Foxworthy ◽  
Patrick I. Eacho
Keyword(s):  
Estrogen Receptor ◽  
Gene Transcription ◽  
Hepatic Lipase ◽  
Lipase Gene ◽  
Hepatic Lipase Gene

scholarly journals Distinct Nongenomic Signal Transduction Pathways Controlled by 17β-Estradiol Regulate DNA Synthesis and Cyclin D1 Gene Transcription in HepG2 Cells

2002 ◽  
Vol 13 (10) ◽  
pp. 3720-3729 ◽  
Author(s):  
Maria Marino ◽  
Filippo Acconcia ◽  
Francesco Bresciani ◽  
Alessandro Weisz ◽  
Anna Trentalance
Keyword(s):  
Gene Expression ◽  
Signal Transduction ◽  
Estrogen Receptor ◽  
Protein Kinase ◽  
Dna Synthesis ◽  
Gene Transcription ◽  
Hepg2 Cells ◽  
Signal Transduction Pathways ◽  
Cyclin D ◽  
17Β Estradiol

Estrogens induce cell proliferation in target tissues by stimulating progression through the G1 phase of the cell cycle. Activation of cyclin D1 gene expression is a critical feature of this hormonal action. The existence of rapid/nongenomic estradiol-regulated protein kinase C (PKC-α) and extracellular signal-regulated kinase (ERK) signal transduction pathways, their cross talk, and role played in DNA synthesis and cyclin D1 gene transcription have been studied herein in human hepatoma HepG2 cells. 17β-Estradiol was found to rapidly activate PKC-α translocation and ERK-2/mitogen-activated protein kinase phosphorylation in this cell line. These actions were independent of each other, preceding the increase of thymidine incorporation into DNA and cyclin D1expression, and did not involve DNA binding by estrogen receptor. The results obtained with specific inhibitors indicated that PKC-α pathway is necessary to mediate the estradiol-induced G1-S progression of HepG2 cells, but it does not exert any effect(s) on cyclin D1 gene expression. On the contrary, ERK-2 cascade was strongly involved in both G1-S progression and cyclin D1gene transcription. Deletion of its activating protein-1 responsive element motif resulted in attenuation of cyclin D1 promoter responsiveness to estrogen. These results indicate that estrogen-induced cyclin D1 transcription can occur in HepG2 cells independently of the transcriptional activity of estrogen receptor, sustaining the pivotal role played by nongenomic pathways of estrogen action in hormone-induced proliferation.

Discovery of NM23-H2 as an estrogen receptor β-associated protein: Role in estrogen-induced gene transcription and cell migration

2008 ◽  
Vol 108 (1-2) ◽  
pp. 72-81 ◽  
Author(s):  
Katey Rayner ◽  
Yong-Xiang Chen ◽  
Benjamin Hibbert ◽  
Dawn White ◽  
Harvey Miller ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Cell Migration ◽  
Gene Transcription ◽  
Estrogen Receptor Β

Regulation by estrogen receptor of vitellogenin gene transcription in Xenopus hepatocyte cultures

1984 ◽  
Vol 38 (2-3) ◽  
pp. 151-161 ◽  
Author(s):  
Andrew J. Perlman ◽  
Alan P. Wolffe ◽  
Janet Champion ◽  
Jamshed R. Tata
Keyword(s):  
Estrogen Receptor ◽  
Gene Transcription ◽  
Hepatocyte Cultures ◽  
Vitellogenin Gene

172 IN VITRO EXPOSURE TO XENOESTROGENS INDUCES GROWTH HORMONE TRANSCRIPTION AND RELEASE VIA AN ESTROGEN RECEPTOR-DEPENDENT PATHWAY IN RAT PITUITARY GH3 CELLS

2008 ◽  
Vol 20 (1) ◽  
pp. 166
Author(s):  
V.-H. Dang ◽  
E.-B. Jeung
Keyword(s):  
Gene Expression ◽  
Growth Hormone ◽  
Estrogen Receptor ◽  
Gene Transcription ◽  
Gh3 Cells ◽  
Pituitary Cells ◽  
Rat Pituitary ◽  
In Vitro Exposure ◽  
Gh Gene

The term endocrine disruptor (ED) has been used widely to characterize natural and synthetic environmental compounds that may interfere with the endocrine system(s) of humans and wildlife. In previous studies, we demonstrated that in vitro single exposure to EDs induces CaBP-9k expression, a useful biomarker for detecting the estrogenic activities of EDs in rat pituitary GH3 cells. Here we employ the identical model to examine the effects of EDs in the regulation of growth hormone (GH) gene expression, an important hormone in growth, development, and body composition. We measured levels of GH mRNA transcription and GH release using semi-quantitative RT-PCR and EIA kit, respectively. GH3 cells were treated with alkyphenols (APs), i.e., octyl-phenol (OP), nonyl-phenol (NP), and bisphenol A (BPA), in a dose-dependent manner (10–5, 10–6, and 10–7 M) and harvested following 24 h of treatment. Cells were also exposed to a high concentration (10–5 M) of OP, NP, or BPA and harvested at various time points (1, 3, 6, 12, and 24 h). An anti-estrogen, ICI 182780 (10–7 M) was used to examine the potential involvement of estrogen receptor (ER) in the induction of GH by EDs through an ER-mediated pathway. The data were analyzed by one-way ANOVA, followed by Tukey's multiple comparison. OP, NP, and BPA induced a significant increase in GH gene expression at high (10–5 M) and medium (10–6 M) doses at 24 h. ED-exposure induced a marked increase in GH gene transcription as early as 6 h and peaked at 12 h. Co-treatment with ICI 182780 significantly attenuated ED-induced GH expression in GH3 cells. Interestingly, the level of in vitro GH release was increased significantly at 24 h in response to OP, NP, or BPA, whereas co-treatment with ICI 182780 significantly diminished ED-induced GH secretion in GH3 cells, indicating that ER may play a part in both GH gene transcription and GH release in these cells. Here we demonstrate for the first time that single in vitro exposure to OP, NP, or BPA results in an increase in GH expression at 24 h in GH3 rat pituitary cells. These results may provide new insight into the mode of ED action in GH gene regulation as well as the biological pathway underlying these molecular events. Furthermore, data showing GH responsiveness evoked by EDs supports the aim to develop an assay for use in predicting adverse health effects of EDs in humans and wildlife.

scholarly journals Classical GenotropicVersusKinase-Initiated Regulation of Gene Transcription by the Estrogen Receptor α

Endocrinology ◽  
2006 ◽  
Vol 147 (4) ◽  
pp. 1986-1996 ◽  
Author(s):  
M. Almeida ◽  
L. Han ◽  
C. A. O’Brien ◽  
S. Kousteni ◽  
S. C. Manolagas
Keyword(s):  
Estrogen Receptor ◽  
Gene Transcription ◽  
Estrogen Receptor Α

scholarly journals Estrogen Response Element-Independent Estrogen Receptor (ER)-α Signaling Does Not Rescue Sexual Behavior but Restores Normal Testosterone Secretion in Male ERα Knockout Mice

Endocrinology ◽  
2007 ◽  
Vol 148 (11) ◽  
pp. 5288-5294 ◽  
Author(s):  
Melissa A. McDevitt ◽  
Christine Glidewell-Kenney ◽  
Jeffrey Weiss ◽  
Pierre Chambon ◽  
J. Larry Jameson ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Sexual Behavior ◽  
Gene Transcription ◽  
Sexual Behaviors ◽  
Elevated Serum ◽  
Normal Male ◽  
Classical Pathway ◽  
Male Reproductive Function ◽  
Estrogen Response ◽  
Regulate Gene

Estrogen receptor (ER)-α mediates estradiol (E2) actions in the male gonads and brain and is critical for normal male reproductive function. In the classical pathway, ERα binds to estrogen response elements (EREs) to regulate gene transcription. ERα can also regulate gene transcription independently of EREs via protein-protein interactions with transcription factors and additionally signal via rapid, nongenomic pathways originating at the cell membrane. This study assessed the degree to which ERE-independent ERα signaling can rescue the disrupted masculine sexual behaviors and elevated serum testosterone (T) levels that have been shown to result from ERα gene deletion. We utilized male ERα null mice that possess a ER knock-in mutation (E207A/G208A; AA), in which the mutant ERα is incapable of binding to DNA and can signal only through ERE-independent pathways (ERα−/AA mice). We found that sexual behavior, including mounting, is virtually absent in ERα−/− and ERα−/AA males, suggesting that ERE-independent signaling is insufficient to maintain any degree of normal sexual behavior in the absence of ERE binding. By contrast, ERE-independent signaling in the ERα−/AA mouse is sufficient to restore serum T levels to values observed in wild-type males. These data indicate that binding of ERs to EREs mediates most if not all of E2’s effects on male sexual behavior, whereas ERE-independent ERα signaling may mediate E2’s inhibitory effects on T production.

Sp1 is essential for estrogen receptor α gene transcription

2002 ◽  
Vol 82 (1) ◽  
pp. 7-18 ◽  
Author(s):  
Linda A. deGraffenried ◽  
Susan G. Hilsenbeck ◽  
Suzanne A.W. Fuqua
Keyword(s):  
Estrogen Receptor ◽  
Gene Transcription ◽  
Estrogen Receptor Α ◽  
Estrogen Receptor Α Gene

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.

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