Critical Role for Estrogen Receptor alpha in Negative Feedback Regulation of Gonadotropin-Releasing Hormone mRNA Expression in the Female Mouse

2003 ◽  
Vol 78 (4) ◽  
pp. 204-209 ◽  
Author(s):  
Amber A. Dorling ◽  
Martin G. Todman ◽  
Kenneth S. Korach ◽  
Allan E. Herbison
Keyword(s):  
Estrogen Receptor ◽  
Mrna Expression ◽  
Negative Feedback ◽  
Female Mouse ◽  
Estrogen Receptor Alpha ◽  
Critical Role ◽  
Feedback Regulation ◽  
Gonadotropin Releasing Hormone ◽  
Negative Feedback Regulation ◽  
Receptor Alpha

Aromatase and estrogen receptor alpha mRNA expression as prognostic biomarkers in patients with astrocytomas

2014 ◽  
Vol 119 (2) ◽  
pp. 275-284 ◽  
Author(s):  
J. M. Dueñas Jiménez ◽  
A. Candanedo Arellano ◽  
A. Santerre ◽  
S. Orozco Suárez ◽  
H. Sandoval Sánchez ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Mrna Expression ◽  
Estrogen Receptor Alpha ◽  
Prognostic Biomarkers ◽  
Receptor Alpha

scholarly journals Estrogen receptor alpha mediates neuronal differentiation and neuroprotection in PC12 cells: critical role of the A/B domain of the receptor

2005 ◽  
Vol 35 (2) ◽  
pp. 257-267 ◽  
Author(s):  
Yohann Mérot ◽  
François Ferrière ◽  
Edith Debroas ◽  
Gilles Flouriot ◽  
Dominique Duval ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Neuronal Differentiation ◽  
Pc12 Cells ◽  
Estrogen Receptor Alpha ◽  
Transcriptional Activity ◽  
Target Genes ◽  
Critical Role ◽  
Full Length ◽  
Receptor Alpha ◽  
Estrogenic Effects

Numerous studies, both in vivo and in vitro, have reported neuronal differentiating and neuroprotective actions of estrogens. Most of these estrogenic effects are mediated through specific receptors termed estrogen receptors. The aim of this study was to assess the importance of the N-terminal A/B domain of the estrogen receptor-alpha (ERα) in its neuronal aspects. Consequently, estrogen effects on (i) the transcriptional activity of target genes, (ii) neuronal differentiation and (iii) neuroprotection in PC12 cells transfected with either a full length form of ERα or an A/B domain truncated form (ERαCF), have been studied. We demonstrate that the maximal estrogen-induced transcriptional activity of reporter genes requires a full length ERα, especially when cells are differentiated. Precisely, the transcriptional activity of ERα in differentiated cells relies, predominantly, on the activation function AF-1, located in the A/B domain. Furthermore, in PC12 cells stably expressing ERα, 17β-estradiol markedly enhances the neurite outgrowth triggered by treatment with nerve growth factor and protects cells from oxidative shocks induced by depletion of glutathione. These estrogenic effects are not observed in non-transfected cells and in cells transfected with the truncated ER, devoid of the A/B domain. Altogether, these results underline the importance of the A/B domain of ERα in both the differentiating and the neuroprotective effects of estrogens.

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