Nuclear estrogen receptor molecular heterogeneity in the mouse uterus.

Golding, Thomas S.; Korach, Kenneth S.

doi:10.1073/pnas.85.1.69

Cited by 38 publications

(15 citation statements)

References 26 publications

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“…These results suggest that the nuclear ER from EGFtreated mice interacts with an ERE in a manner similar to that observed after estrogen treatment. It has previously been demonstrated that estrogen treatment induces heterogenous nuclear ER forms of 65-and 66.5-kDa in uterine nudear extracts (22) and that the 66.5-kDa form is hyperphosphorylated ER (24). Similar to the effect of estrogen, EGF treatment elicited the formation of the unique nuclear 66.5-kDa form of ER as assessed by immunodetection with H222 antibody.…”

Section: Introductionmentioning

confidence: 88%

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Cross talk between peptide growth factor and estrogen receptor signaling systems.

Ignar-Trowbridge

Pimentel

Teng

et al. 1995

Environ Health Perspect

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Epidermal growth factor reproduces many of the effects of estrogen on the murine female reproductive tract and may partially mediate estrogen-induced growth and differentiation. The mechanism by which the actions of estrogens and epidermal growth factor (EGF) converge is unknown. The studies described herein were performed to investigate the possibility that some of the actions of EGF may be mediated through the estrogen receptor. A specific estrogen receptor (ER) antagonist inhibited estrogenlike effects of EGF in the mouse uterus, specifically induction of DNA synthesis and phosphatidylinositol turnover. In addition, EGF elicited enhanced nuclear localization of uterine ER and formation of a unique nuclear form of ER that is present after estrogen treatment. These in vivo observations indicated that EGF may elicit some of its actions by activation of nuclear ER. Thus, the effect of peptide growth factors on activation of a consensus estrogen response element was assessed in Ishikawa human endometrial adenocarcinoma cells, which contain negligible ER levels, and in BG-1 human ovarian adenocarcinoma cells, which contain abundant ER. EGF and TGFa induced transcriptional activation of a consensus estrogen response element (ERE) in an ER-dependent manner in both cell types. In addition, insulinlike growth factor (IGF-1) was as potent as 17,B-estradiol in BG-1 cells. Synergism between growth factors and estrogen was observed in both cell types, although synergism was not observed between the different classes of growth factors [i.e., transforming growth factor a (TGFa) and IGF-Il in BG-1 cells. The most potent activator of ERE-dependent transcription was a protein kinase C activator (TPA), which acted synergistically with 1 7festradiol. A protein kinase C inhibitor abolished the effect of TPA but not that of 1 7festradiol, IGF-I, or TGFa. A protein kinase A activator elicited ER-dependent activation of transcription and did not synergize with estrogen or growth factors. In conclusion, some physiologic actions of peptide growth factors are dependent on ER. Indeed, growth factors are capable of eliciting ER-dependent activation of an ERE. Both the protein kinase A and protein kinase C pathways can elicit ER-dependent transcriptional activation; however, it is unlikely that these pathways mediate the effects of peptide growth factors on the ER in BG-1 cells. -Environ Health Perspect 1 03(Suppl 7): 35-38 (1995)

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Section: Introductionmentioning

confidence: 88%

“…Estrogen treatment rapidly enhances ER affinity for chromatin so that the ER is retained in the nuclear fraction after tissue homogenization. This phenomenon is quantitated by a 3H-estradiol-binding assay (21,22). Significant augmentation of nuclear ER levels was observed 1.5 hr after EGF pellet implantation or DES treatment.…”

Section: Introductionmentioning

confidence: 99%

Cross talk between peptide growth factor and estrogen receptor signaling systems.

Ignar-Trowbridge

Pimentel

Teng

et al. 1995

Environ Health Perspect

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“…Estrogen treatment rapidly enhances ER affinity for chromatin so that the ER is retained in the nuclear fraction after tissue homogenization. This phenomenon can be quantitated by a [3H]estradiol binding assay (18,19). As shown in Fig.…”

mentioning

confidence: 99%

“…The [3H]estradiol binding assay was performed as described (18) with modifications (19). Uterine tissue was homogenized in ice-cold TEGM buffer and the nuclear pellet was washed twice in this buffer.…”

mentioning

confidence: 99%

Coupling of dual signaling pathways: epidermal growth factor action involves the estrogen receptor.

Ignar-Trowbridge

Nelson

Bidwell

et al. 1992

Proc. Natl. Acad. Sci. U.S.A.

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456

218

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Epidermal growth factor (EGF) reproduces many of the effects of estrogen on the murine female reproductive tract and may partially mediate estroged-induced growth and differentiation. This study was performed to investigate the mechanism by which EGF elicits estrogen-like actions in the whole animal. EGF was ad tered to adult ovariectomized mice by slow release pellets implanted under the kidney capsule. The induction ofuterine DNA synthesis and phosphatidylinositol lipid turnover by EGF or admintation of diethylstilbestrol (5 pg/kg), a potent estrogen, was attenuated by the estrogen receptor antagonist ICI 164,384. Furthermore, EGF mimicked the effects of estrogen on enhanced nuclear localization of the estrogen receptor and the formation of a unique form of the estrogen receptor found exclusively in the nucleus. These results suggest that EGF may induce effects similar to those of estrogen in the mouse uterus by an interaction between the EGF signaling pathway and the classical estrogen receptor. The demonstration of cross-talk between polypeptide growth factors and steroid hormone receptors may be of importance to our understanding of the regulation of normal growth and differentiation as well as the mechanisms of transmission of extracellular mitogen signals to the nucleus.It has been proposed that polypeptide growth factors may act as autocrine or paracrine mediators of estrogen-induced mitogenesis (1, 2). The observations that estrogen induces mRNA and protein for both epidermal growth factor (EGF) (3,4) and its receptor (5-7) in rodent uterus are consistent with this hypothesis and implicate a role for the EGF receptor signaling pathway in steroid hormone regulation of uterine tract growth. Furthermore, exogenous EGF administration to adult ovariectomized mice mimics the effects of estrogen on proliferation and differentiation in the murine female reproductive tract (8). EGF-induced mitogenesis in this model is not affected by adrenalectomy or hypophysectomy, which indicates that adrenal or pituitary hormones do not mediate the effects of EGF. In addition, the fact that an EGF-specific antibody administered prior to estradiol partially blocks estrogen-induced uterine epithelial cell proliferation (8) suggests that production of EGF may be necessary for estrogen-induced responses.Presently, the mechanism by which the actions of estrogens and EGF converge is unknown. This study addresses the intriguing possibility that some of the physiological actions of EGF, an extracellular ligand, may be mediated through a nuclear steroid hormone receptor, namely, the estrogen receptor (ER). Two recent reports by Power et al. (9,10) support such a hypothesis. These studies demonstrated that dopamine, an extracellular ligand, was able to stimulate transcriptional enhancement by three members of the steroid receptor superfamily [the progesterone receptor (PR), ER, and COUP (chicken ovalbumin upstream promoter) transcriptional enhancer], which were transfected into CV1 monkey kidney cells. Furthermore, in MCF-7 hu...

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“…Aliquots of each are assayed for [ 3 H]-estradiol or [ 3 H]-4-hydroxyestradiol binding as described previously (61). For normalization of binding data, DNA content of the nuclear fraction is measured using the procedure of Labarca and Paigen (62).…”

Section: Labeling and Purification Of Catechol Estrogensmentioning

confidence: 99%

Breast Cancer Associated Estrogen Receptors: Catechol Estrogen Receptors in ER-Minus Mice

Lubahn¹

1999

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Nuclear estrogen receptor molecular heterogeneity in the mouse uterus.

Cited by 38 publications

References 26 publications

Cross talk between peptide growth factor and estrogen receptor signaling systems.

Cross talk between peptide growth factor and estrogen receptor signaling systems.

Coupling of dual signaling pathways: epidermal growth factor action involves the estrogen receptor.

Breast Cancer Associated Estrogen Receptors: Catechol Estrogen Receptors in ER-Minus Mice

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