Estrogen Receptor Subtypes ERalpha and ERbeta May Have Overlapping Roles in Oocyte Development.

2010 ◽  
Vol 83 (Suppl_1) ◽  
pp. 180-202
Author(s):  
Fangjie Tang ◽  
Melissa E. Pepling
Endocrinology ◽  
1999 ◽  
Vol 140 (9) ◽  
pp. 4320-4334 ◽  
Author(s):  
S. Chidananda Sharma ◽  
Jeffrey W. Clemens ◽  
Margareta D. Pisarska ◽  
JoAnne S. Richards

2008 ◽  
Vol 196 (1) ◽  
pp. 49-58 ◽  
Author(s):  
Maria Natalia Cruz ◽  
Stefan Agewall ◽  
Karin Schenck-Gustafsson ◽  
Karolina Kublickiene

Tumor Biology ◽  
2014 ◽  
Vol 35 (9) ◽  
pp. 9111-9117 ◽  
Author(s):  
Weiliang Sun ◽  
Chijiang Gu ◽  
Minming Xia ◽  
Guoping Zhong ◽  
Haojun Song ◽  
...  

2010 ◽  
Vol 2010 ◽  
pp. 1-14 ◽  
Author(s):  
E. Kassi ◽  
P. Moutsatsou

Dysregulation of cytokines is among the main abnormalities in Systemic Lupus Erythematosus (SLE). However, although, estrogens, which are known to be involved in lupus disease, influence cytokine production, the underlying molecular mechanisms remain poorly defined. Recent evidence demonstrates the presence of estrogen receptor in various cell types of the immune system, while divergent effects of estrogens on the cytokine regulation are thought to be implicated. In this paper, we provide an overview of the current knowledge as to how estrogen-induced modulation of cytokine production in SLE is mediated by the estrogen receptor while simultaneously clarifying various aspects of estrogen receptor signaling in this disease. The estrogen receptor subtypes, their structure, and the mode of action of estrogens by gene activation and via extranuclear effects are briefly presented. Results regarding the possible correlation between estrogen receptor gene polymorphisms and quantitative changes in the receptor protein to SLE pathology and cytokine production are reviewed.


2019 ◽  
Author(s):  
Min Hu ◽  
Yuehui Zhang ◽  
Emil Egecioglu ◽  
Xin Li ◽  
Linus Shao ◽  
...  

2019 ◽  
Vol 41 (3-4) ◽  
pp. 203-211 ◽  
Author(s):  
Yu-xiang Wang ◽  
Lin Zhu ◽  
Li-xia Li ◽  
Hui-nan Xu ◽  
Hong-gang Wang ◽  
...  

The Papez circuit is crucial for several brain functions, including long-term memory and emotion. Estradiol modulates cognitive functions based on the expression pattern of its receptor subtypes including estrogen receptor (ER) α, β, and G protein-coupled receptor 30 (GPR30). Similarly, the activity in the cholinergic system correlates with several brain functions, such as learning and memory. In this study, we used immunofluorescence to examine the expression patterns of ERβ and Western blotting to analyze GPR30 and choline acetyltransferase (ChAT) expression, in different regions of the Papez circuit, including the prefrontal cortex, hippocampus, hypothalamus, anterior nucleus of the thalamus, and cingulum in female rats at postnatal days (PND) 1, 10, and 56. Our main finding was that the highest expression of ERβ and GPR30 was noted in each brain area of the Papez circuit in the PND1 rats, whereas the expression of ChAT was the highest in PND10 rats. These results provide vital information on the postnatal expression patterns of ER subtypes and ChAT in different regions of the Papez circuit.


2000 ◽  
Vol 279 (3) ◽  
pp. H1208-H1214 ◽  
Author(s):  
M. T. Littleton-Kearney ◽  
D. M. Agnew ◽  
R. J. Traystman ◽  
P. D. Hurn

We tested the hypothesis that intracarotid estrogen infusion increases cerebral blood flow (CBF) in a concentration-dependent manner and direct application of estrogen on pial arterioles yields estrogen receptor-mediated vasodilation. Rabbits of both genders were infused with estrogen via a branch of the carotid artery. Estrogen doses of 20 or 0.05 μg · ml−1 · min−1 were used to achieve supraphysiological or physiological plasma estrogen levels, respectively. CBF and cerebral vascular resistance were determined at baseline, during the infusion, and 60-min postinfusion, and effects on pial diameter were assessed via a cranial window. Pial arteriolar response to estrogen alone and to estrogen after administration of tamoxifen (10−7), an antiestrogen drug that binds to both known estrogen receptor subtypes, was tested. No gender differences were observed; therefore, data were combined for both males and females. Systemic estrogen infusion did not increase regional CBF. Estradiol dilated pial arteries only at concentrations ranging from 10−4–10−7 M ( P ≤ 0.05). Pretreatment with tamoxifen alone had no effect on arteriolar diameter but inhibited estrogen-induced vasodilation ( P < 0.001). Our data suggest that estrogen does not increase CBF under steady-state conditions in rabbits. In the pial circulation, topically applied estradiol at micromolar concentrations dilates vessels. The onset is rapid and dependent on estrogen receptor activation.


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