Antidepressants do not modulate estrogen receptor α-mediated gene expression

2001 ◽  
Vol 108 (10) ◽  
pp. 1197-1202 ◽  
Author(s):  
B. Hermann ◽  
I. Vollmer ◽  
F. Holsboer ◽  
R. Rupprecht
Keyword(s):  
Gene Expression ◽  
Estrogen Receptor ◽  
Estrogen Receptor Α

scholarly journals Loading-related regulation of gene expression in bone in the contexts of estrogen deficiency, lack of estrogen receptor α and disuse

Bone ◽  
2010 ◽  
Vol 46 (3) ◽  
pp. 628-642 ◽  
Author(s):  
Gul Zaman ◽  
Leanne K. Saxon ◽  
Andrew Sunters ◽  
Helen Hilton ◽  
Peter Underhill ◽  
...  
Keyword(s):  
Gene Expression ◽  
Estrogen Receptor ◽  
Regulation Of Gene Expression ◽  
Estrogen Receptor Α ◽  
Estrogen Deficiency

G-protein Coupled Estrogen Receptor Expression in Growth Hormone Secreting and Non-Functioning Adenomas

2020 ◽  
Author(s):  
Hande Mefkure Ozkaya ◽  
Muge Sayitoglu ◽  
Nil Comunoglu ◽  
Eda Sun ◽  
Fatma Ela Keskin ◽  
...  
Keyword(s):  
Gene Expression ◽  
Estrogen Receptor ◽  
Protein Expression ◽  
G Protein ◽  
Estrogen Receptor Α ◽  
Receptor Expression ◽  
Positive Correlation ◽  
Polymerase Chain ◽  
G Protein Coupled ◽  
Transforming Gene

Abstract Purpose To evaluate the expression of G-protein coupled estrogen receptor (GPER1), aromatase, estrogen receptor α (ERα), estrogen receptor β (ERβ), pituitary tumor transforming gene (PTTG), and fibroblast growth factor 2 (FGF2) in GH-secreting and non-functioning adenomas (NFA). Methods Thirty patients with acromegaly and 27 patients with NFA were included. Gene expression was determined via quantitative reverse transcription polymerase chain reaction (QRT-PCR). Protein expression was determined via immunohistochemistry. Results There was no difference, in terms of gene expression of aromatase, ERα, PTTG, and FGF2 between the two groups (p>0.05 for all). ERβ gene expression was higher and GPER1 gene expression was lower in GH-secreting adenomas than NFAs (p<0.05 for all). Aromatase and ERβ protein expression was higher in GH-secreting adenomas than NFAs (p=0.01). None of the tumors expressed ERα. GPER1 expression was detected in 62.2% of the GH-secreting adenomas and 45% of NFAs. There was no difference in terms of GPER1, PTTG, FGF2 H scores between the two groups (p>0.05 for all). GPER1 gene expression was positively correlated to ERα, ERβ, PTTG, and FGF2 gene expression (p<0.05 for all). There was a positive correlation between aromatase and GPER1 protein expression (r=0.31; p=0.04). Conclusions GPER1 is expressed at both gene and protein level in a substantial portion of GH-secreting adenomas and NFAs. The finding of a positive correlation between GPER1 and ERα, ERβ, PTTG, and FGF2 gene expression and aromatase and GPER1 protein expression suggests GPER1 along with aromatase and classical ERs might mediate the effects of estrogen through upregulation of PTTG and FGF2.

scholarly journals GRIP1 enhances estrogen receptor α-dependent extracellular matrix gene expression in chondrogenic cells

2010 ◽  
Vol 18 (7) ◽  
pp. 934-941 ◽  
Author(s):  
M. Kato ◽  
H. Takaishi ◽  
M. Yoda ◽  
T. Tohmonda ◽  
J. Takito ◽  
...  
Keyword(s):  
Gene Expression ◽  
Extracellular Matrix ◽  
Estrogen Receptor ◽  
Estrogen Receptor Α ◽  
Matrix Gene

scholarly journals Estradiol Stimulates Apolipoprotein A-IV Gene Expression in the Nucleus of the Solitary Tract Through Estrogen Receptor-α

Endocrinology ◽  
2014 ◽  
Vol 155 (10) ◽  
pp. 3882-3890 ◽  
Author(s):  
Ling Shen ◽  
Yin Liu ◽  
David Q.H. Wang ◽  
Patrick Tso ◽  
Stephen C. Woods ◽  
...  
Keyword(s):  
Gene Expression ◽  
Estrogen Receptor ◽  
Nucleus Tractus Solitarius ◽  
Body Weight Gain ◽  
Gene Promoter ◽  
Estrogen Receptor Α ◽  
Inhibitory Effect ◽  
Female Rats ◽  
Upstream Region ◽  
Apolipoprotein A

Abstract Although estrogens have been implicated in the regulation of apolipoprotein A-IV (apo A-IV) gene expression in the nucleus tractus solitarius, previous studies have not defined the molecular mechanism. The aim of this study was to examine the transcriptional mechanisms involved in regulation of apo A-IV gene expression. Using cultured primary neuronal cells from rat embryonic brainstems, we found that treatment with 10nM 17β-estradiol-3-benzoate (E2) or 4,4′,4″-(4-propyl-[1H]-pyrazole-1,3,5-triyl) trisphenol (an estrogen receptor [ER]α agonist), but not 2,3-bis(4-hydroxyphenyl)-propionitrile (an ERβ agonist), significantly increased apo A-IV gene expression, compared with vehicle treatment. This effect of E2 was abolished when the cells were incubated with E2 linked to BSA, which prevents E2 from entering cells, implying that a nongenomic mechanism of E2 is not involved. Two putative estrogen response elements were identified at the 5′-upstream region of the apo A-IV gene promoter, but only 1 of them was able to recruit ERα, leading to increased apo A-IV gene expression, as determined by chromatin immunoprecipitation assay and luciferase activity analysis. A cyclic regimen of E2 or 4,4′,4″-(4-propyl-[1H]-pyrazole-1,3,5-triyl) trisphenol treatment for 8 cycles (4 d/cycle, mimicking the ovarian cycle of female rats) in ovariectomized female rats significantly reduced food intake and body weight gain and increased apo A-IV gene expression in the nucleus tractus solitarius, relative to vehicle. These data collectively demonstrate that nuclear ERα is the primary mediator of E2's action on apo A-IV gene expression and suggest that increased signaling of endogenous apo A-IV may at least partially mediate E2-induced inhibitory effect on feeding.

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