17β-Estradiol Stimulates Mouse Neuropeptide Y-Y1 Receptor Gene Transcription by Binding to Estrogen Receptor Alpha in Neuroblastoma Cells

2000 ◽  
Vol 72 (6) ◽  
pp. 360-367 ◽  
Author(s):  
Rita Musso ◽  
Adriana Maggi ◽  
Carola Eva
Keyword(s):  
Estrogen Receptor ◽  
Neuropeptide Y ◽  
Gene Transcription ◽  
Estrogen Receptor Alpha ◽  
Receptor Gene ◽  
Neuroblastoma Cells ◽  
Receptor Alpha ◽  
17Β Estradiol

scholarly journals Equol Pretreatment Protection of SH-SY5Y Cells against Aβ (25–35)-Induced Cytotoxicity and Cell-Cycle Reentry via Sustaining Estrogen Receptor Alpha Expression

Nutrients ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 2356 ◽  
Author(s):  
Meng-Chao Tsai ◽  
Shyh-Hsiang Lin ◽  
Kiswatul Hidayah ◽  
Ching-I Lin
Keyword(s):  
Cell Cycle ◽  
Estrogen Receptor ◽  
Estrogen Receptor Alpha ◽  
Biological Effects ◽  
Neuroblastoma Cells ◽  
Amyloid Formation ◽  
Receptor Alpha ◽  
Cell Cycle Reentry ◽  
Extracellular Signal ◽  
17Β Estradiol

β-amyloid formation in the brain is one of the characteristics of Alzheimer’s disease. Exposure to this peptide may result in reentry into the cell cycle leading to cell death. The phytoestrogen equol has similar biological effects as estrogen without the side effects. This study investigated the possible mechanism of the neuron cell-protecting effect of equol during treatment with Aβ. SH-SY5Y neuroblastoma cells were treated with either 1 μM S-equol or 10 nM 17β-estradiol for 24 h prior to 1 μM Aβ (25–35) exposure. After 24 h exposure to Aβ (25–35), a significant reduction in cell survival and a reentry into the cell cycle process accompanied by increased levels of cyclin D1 were observed. The expressions of estrogen receptor alpha (ERα) and its coactivator, steroid receptor coactivator-1 (SRC-1), were also significantly downregulated by Aβ (25–35) in parallel with activated extracellular signal-regulated kinase (ERK)1/2. However, pretreatment of cells with S-equol or 17β-estradiol reversed these effects. Treatment with the ER antagonist, ICI-182,780 (1 μM), completely blocked the effects of S-equol and 17β-estradiol on cell viability, ERα, and ERK1/2 after Aβ (25–35) exposure. These data suggest that S-equol possesses a neuroprotective potential as it effectively antagonizes Aβ (25–35)-induced cell cytotoxicity and prevents cell cycle reentry in SH-SY5Y cells. The mechanism underlying S-equol neuroprotection might involve ERα-mediated pathways.

17β-Estradiol and/or estrogen receptor alpha blocks isoproterenol-induced calcium accumulation and hypertrophy via GSK3β/PP2A/NFAT3/ANP pathway

2017 ◽  
Vol 434 (1-2) ◽  
pp. 181-195 ◽  
Author(s):  
Peiying Pai ◽  
Bharath Kumar Velmurugan ◽  
Chia-Hua Kuo ◽  
Chung-Yi Yen ◽  
Tsung-Jung Ho ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Alpha ◽  
Receptor Alpha ◽  
Calcium Accumulation ◽  
17Β Estradiol

scholarly journals Regulation of estrogen receptor-alpha expression in MCF-7 cells by taxol

2004 ◽  
Vol 180 (3) ◽  
pp. 487-496 ◽  
Author(s):  
MB Martin ◽  
SV Angeloni ◽  
P Garcia-Morales ◽  
PF Sholler ◽  
MD Castro-Galache ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Progesterone Receptor ◽  
Gene Transcription ◽  
Estrogen Receptor Alpha ◽  
Receptor Protein ◽  
Subsequent Increase ◽  
Receptor Alpha ◽  
Alpha Gene ◽  
Er Alpha ◽  
Mcf 7

Results presented in this study demonstrate that treatment of MCF-7 cells with taxol resulted in induction of estrogen receptor-alpha (ER alpha) gene transcription with a subsequent increase in ER alpha mRNA; this effect was promoter specific since taxol did not affect total transcription in MCF-7 cells and lacked an effect on transcription of the human acidic ribosomal phosphoprotein protein PO, progesterone receptor, and pS2 genes. In contrast to the increase in transcription of the ER alpha gene, taxol inhibited translation of the ER alpha mRNA. This effect is also transcript specific since taxol did not alter total protein synthesis and did not affect the concentration of progesterone receptor protein in the cell. The overall result of taxol treatment was to decrease the concentration of ER alpha protein in the MCF-7 cells. Evidence is presented that the effects of taxol on ER alpha gene transcription may be mediated through the induction of p53.

scholarly journals 17β-Estradiol Prevents Early-Stage Atherosclerosis in Estrogen Receptor-Alpha Deficient Female Mice

2009 ◽  
Vol 2 (3) ◽  
pp. 289-299 ◽  
Author(s):  
Amparo C. Villablanca ◽  
Amy Tenwolde ◽  
Michael Lee ◽  
Melissa Huck ◽  
Shannon Mumenthaler ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Alpha ◽  
Early Stage ◽  
Receptor Alpha ◽  
Female Mice ◽  
17Β Estradiol

scholarly journals Physiologically Relevant Estrogen Receptor Alpha Pathway Reporters for Single-Cell Imaging-Based Carcinogenic Hazard Assessment of Estrogenic Compounds

2021 ◽  
Author(s):  
Britt Duijndam ◽  
Annabel Goudriaan ◽  
Tineke van den Hoorn ◽  
Wanda van der Stel ◽  
Sylvia Le Dévédec ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Single Cell ◽  
Cell Lines ◽  
Estrogen Receptor Alpha ◽  
Target Genes ◽  
Dependent Manner ◽  
Reporter Cell ◽  
Estrogenic Compounds ◽  
Receptor Alpha ◽  
17Β Estradiol

Abstract Estrogen receptor alpha (ERα) belongs to the nuclear hormone receptor family of ligand-inducible transcription factors and regulates gene networks in biological processes such as cell growth and proliferation. Disruption of these networks by chemical compounds with estrogenic activity can result in adverse outcomes such as unscheduled cell proliferation, ultimately culminating in tumor formation. To distinguish disruptive activation from normal physiological responses, it is essential to quantify relationships between different key events leading to a particular adverse outcome. For this purpose, we established fluorescent protein MCF7 reporter cell lines for ERα-induced proliferation by bacterial artificial chromosome-based tagging of 3 ERα target genes: GREB1, PGR, and TFF1. These target genes are inducible by the non-genotoxic carcinogen and ERα agonist 17β-estradiol in an ERα-dependent manner and are essential for ERα-dependent cell-cycle progression and proliferation. The 3 GFP reporter cell lines were characterized in detail and showed different activation dynamics upon exposure to 17β-estradiol. In addition, they demonstrated specific activation in response to other established reference estrogenic compounds of different potencies, with similar sensitivities as validated OECD test methods. This study shows that these fluorescent reporter cell lines can be used to monitor the spatial and temporal dynamics of ERα pathway activation at the single-cell level for more mechanistic insight, thereby allowing a detailed assessment of the potential carcinogenic activity of estrogenic compounds in humans.

scholarly journals 17β-Estradiol and/or estrogen receptor alpha signaling blocks protein phosphatase 1 mediated ISO induced cardiac hypertrophy

PLoS ONE ◽  
2018 ◽  
Vol 13 (5) ◽  
pp. e0196569 ◽  
Author(s):  
Hsin-Yuan Fang ◽  
Meng-Yu Hung ◽  
Yueh-Min Lin ◽  
Sudhir Pandey ◽  
Chia-Chien Chang ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Cardiac Hypertrophy ◽  
Protein Phosphatase ◽  
Estrogen Receptor Alpha ◽  
Protein Phosphatase 1 ◽  
Receptor Alpha ◽  
17Β Estradiol

The effects of 17β-estradiol on blood brain barrier integrity in the absence of the estrogen receptor alpha; an in-vitro model

2017 ◽  
Vol 119 (6) ◽  
pp. 638-647 ◽  
Author(s):  
Serap Erdem Kuruca ◽  
Sabriye Karadenizli ◽  
Kadriye Akgun-Dar ◽  
Aysegul Kapucu ◽  
Zulal Kaptan ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Blood Brain Barrier ◽  
Estrogen Receptor Alpha ◽  
In Vitro Model ◽  
Barrier Integrity ◽  
Receptor Alpha ◽  
17Β Estradiol ◽  
Vitro Model ◽  
Blood Brain Barrier Integrity
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