Immunocytochemistry Versus Binding Assays of the Estrogen Receptor in the Reproductive Tract of Spayed and Hormone-Treated Macaques*

Endocrinology ◽  
1987 ◽  
Vol 121 (5) ◽  
pp. 1789-1800 ◽  
Author(s):  
NEAL B. WEST ◽  
MARYANNE C. McCLELLAN ◽  
MARK D. STERNFELD ◽  
ROBERT M. BRENNER
Keyword(s):  
Estrogen Receptor ◽  
Reproductive Tract ◽  
Binding Assays

scholarly journals Estrogenicity of styrene oligomers and assessment of estrogen receptor binding assays.

2002 ◽  
Vol 110 (7) ◽  
Author(s):  
Katsutoshi Ohno ◽  
Yukimasa Azuma ◽  
Katsuhiro Date ◽  
Shigeru Nakano ◽  
Toru Kobayashi ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Receptor Binding ◽  
Binding Assays ◽  
Estrogen Receptor Binding

scholarly journals Quantitative Analysis of Estrogen Receptor Proteins in Rat Mammary Gland*

Endocrinology ◽  
2001 ◽  
Vol 142 (7) ◽  
pp. 3177-3186 ◽  
Author(s):  
Shigehira Saji ◽  
Hideki Sakaguchi ◽  
Sandra Andersson ◽  
Margaret Warner ◽  
Jan-Åke Gustafsson
Keyword(s):  
Estrogen Receptor ◽  
Mammary Gland ◽  
Total Protein ◽  
Messenger Rna ◽  
Estrogen Receptor Α ◽  
Lactation Period ◽  
Binding Assays ◽  
Western Blots ◽  
Mean Values ◽  
Rat Mammary Gland

Abstract Estrogen receptor α and β proteins (ERα and ERβ) at various stages of development of the rat mammary gland were quantified by Western blotting. ERα and ERβ recombinant proteins were used as standards, and their molar concentrations were measured by ligand binding assays. In 3-week-old pregnant, lactating, and postlactating rats the ERα content ranged from 0.30–1.55 fmol/μg total protein (mean values). The ERβ content of the same samples ranged between 1.06–7.50 fmol/μg total protein. At every developmental stage, the ERβ content of the mammary gland was higher than that of ERα. When receptor levels were normalized against β-actin, it was evident that ER expression changed during development, with maximum expression of both receptors during the lactation period. With an antibody raised against the 18-amino acid insert of the ERβ variant, originally called ERβ2 but named ERβins in this paper, Western blots revealed that ERβins protein was up-regulated during the lactation period. RT-PCR showed that the levels of messenger RNA of ERβins paralleled those of the protein. Double immunohistochemical staining with anti-ERα and anti-ERβins antibodies revealed that ERβins protein colocalized with ERα in 70–80% of the ERα-expressing epithelial cells during lactation and with 30% of these cells during pregnancy. These observations indicate that expression of ERβins is regulated not only quantitatively, but also with regard to its cellular distribution. As ERβins acts as the dominant repressor of ERα, we suggest that its coexpression with ERα quenches ERα function and may be one of the factors that contribute to the previously described insensitivity of the mammary gland to estrogens during lactation.

scholarly journals Responsiveness of endometrial genes Connexin26, Connexin43, C3 and clusterin to primary estrogen, selective estrogen receptor modulators, phyto- and xenoestrogens

2002 ◽  
Vol 29 (2) ◽  
pp. 239-249 ◽  
Author(s):  
S Heikaus ◽  
E Winterhager ◽  
O Traub ◽  
R Grummer
Keyword(s):  
Estrogen Receptor ◽  
Reproductive Tract ◽  
Polychlorinated Biphenyl ◽  
Estrogenic Activity ◽  
Selective Estrogen Receptor Modulators ◽  
Complement C3 ◽  
Estrogen Receptor Modulators ◽  
Industrial Compounds ◽  
Receptor Modulators

Phytohormones and chemical compounds revealing estrogenic effects are of increasing interest for their possible influence on the physiology of the reproductive tract. The gap junction connexin (Cx) genes Cx26 and Cx43, the plasma glycoprotein clusterin gene and the complement C3 gene are highly regulated by estrogen in rat endometrium. To test the value of these genes as markers for estrogenic responsiveness we analyzed the effects of estradiol, diethylstilbestrol, the selective estrogen receptor modulators (SERMs) raloxifene and tamoxifen, the phytoestrogens genistein and daidzein, and the industrial compounds DDT (1,1,1-trichloro-2-(2-chlorophenyl)-2-(4-chlorophenyl) ethane) and polychlorinated biphenyl (PCB) on the transcription of these genes in rat endometrium in vivo. Enhancement of Cx26 and decrease of clusterin transcripts expression by estradiol was observed at 0.03 micro g/250 g body weight (BW), and induction of C3 expression was observed at 0.05 micro g/250 g BW. A comparable effect was obtained by a tenfold higher concentration of diethylstilbestrol. Tamoxifen had a regulatory effect on this set of genes at about a 300-fold higher concentration, while raloxifen revealed much weaker estrogenic activity. No effect on Cx43 transcripts was observed with any of the compounds at the concentrations used. An effect of genistein was observed only on Cx26 expression, while PCB decreased clusterin transcripts. These results show that Cx26, C3 and clusterin reveal a comparable sensitivity to estrogens and SERMs. With respect to the phytoestrogen genistein, however, Cx26 seems to be the most sensitive gene. The analysis of clusters of estrogen-sensitive endometrial genes could help to identify estrogenic substances, assess their potency, and elucidate their mechanism of action.

scholarly journals Similarities and differences in uterine gene expression patterns caused by treatment with physiological and non-physiological estrogens

2003 ◽  
Vol 31 (3) ◽  
pp. 487-497 ◽  
Author(s):  
H Watanabe ◽  
A Suzuki ◽  
M Kobayashi ◽  
DB Lubahn ◽  
H Handa ◽  
...  
Keyword(s):  
Gene Expression ◽  
Estrogen Receptor ◽  
Reproductive Tract ◽  
Stress Proteins ◽  
Expression Patterns ◽  
Gene Expression Patterns ◽  
Response Patterns ◽  
Genes Encoding ◽  
The Many ◽  
Dose Responses

Administration of physiological and non-physiological estrogens during pregnancy or after birth is known to have adverse effects on the development of the reproductive tract and other organs. Although it is believed that both estrogens have similar effects on gene expression, this view has not been tested systematically. To compare the effects of physiological (estradiol; E2) and non-physiological (diethylstilbestrol; DES) estrogens, we used DNA microarray analysis to examine the uterine gene expression patterns induced by the two estrogens. Although E2 and DES induced many genes to respond in the same way, different groups of genes showed varying levels of maximal activities to each estrogen, resulting in different dose-response patterns. Thus, each estrogen has a distinct effect on uterine gene expression. The genes were classified into clusters according to their dose-responses to the two estrogens. Of the eight clusters, only two correlated well with the uterotropic effect of different doses of E2. One of these clusters contained genes that were upregulated by E2, which included genes encoding several stress proteins and transcription factors. The other cluster contained genes that were downregulated by E2, including genes related to metabolism, transcription and detoxification processes. The expression of these genes in estrogen receptor-deficient mice was not affected by E2 treatment, indicating that these genes are affected by the E2-bound estrogen receptor. Thus, of the many genes that are affected by estrogen, it was suggested that only a small number are directly involved in the uterotropic effects of estrogen treatment.

Comparative distribution of estrogen receptor-α (ER-α) and β (ER-β) mRNA in the rat pituitary, gonad, and reproductive tract

Steroids ◽  
1998 ◽  
Vol 63 (10) ◽  
pp. 498-504 ◽  
Author(s):  
Paul J. Shughrue ◽  
Malcolm V. Lane ◽  
Paul J. Scrimo ◽  
Istvan Merchenthaler
Keyword(s):  
Estrogen Receptor ◽  
Reproductive Tract ◽  
Estrogen Receptor Α ◽  
Rat Pituitary

Membrane and Nuclear Estrogen Receptor Alpha Actions: From Tissue Specificity to Medical Implications

2017 ◽  
Vol 97 (3) ◽  
pp. 1045-1087 ◽  
Author(s):  
Jean-Francois Arnal ◽  
Françoise Lenfant ◽  
Raphaël Metivier ◽  
Gilles Flouriot ◽  
Daniel Henrion ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Alpha ◽  
Reproductive Tract ◽  
Vascular System ◽  
Physiological Role ◽  
Receptor Alpha ◽  
Nuclear Signaling ◽  
Nuclear Estrogen Receptor

Estrogen receptor alpha (ERα) has been recognized now for several decades as playing a key role in reproduction and exerting functions in numerous nonreproductive tissues. In this review, we attempt to summarize the in vitro studies that are the basis of our current understanding of the mechanisms of action of ERα as a nuclear receptor and the key roles played by its two activation functions (AFs) in its transcriptional activities. We then depict the consequences of the selective inactivation of these AFs in mouse models, focusing on the prominent roles played by ERα in the reproductive tract and in the vascular system. Evidence has accumulated over the two last decades that ERα is also associated with the plasma membrane and activates non-nuclear signaling from this site. These rapid/nongenomic/membrane-initiated steroid signals (MISS) have been characterized in a variety of cell lines, and in particular in endothelial cells. The development of selective pharmacological tools that specifically activate MISS and the generation of mice expressing an ERα protein impeded for membrane localization have begun to unravel the physiological role of MISS in vivo. Finally, we discuss novel perspectives for the design of tissue-selective ER modulators based on the integration of the physiological and pathophysiological roles of MISS actions of estrogens.

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