Regulation of uterine epidermal growth factor (EGF) receptors by estrogen in the mature rat and during the estrous cycle

Gardner, Russell; Verner, G.; Kirkland, John L.; Stancel, George M.

doi:10.1016/0022-4731(89)90205-7

Cited by 82 publications

(44 citation statements)

References 17 publications

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“…The observations that estrogen induces mRNA and protein for peptide growth factors [epidermal growth factor (EGF), transforming growth factor a (TGFa), and insulinlike growth factor I (IGF-I)] (3-7) and their receptors (8)(9)(10)(11) EGF receptor-signaling pathway in steroid hormone regulation of uterine biology. Our laboratory has previously demonstrated a convergence between the actions of EGF and estradiol in the mouse uterus.…”

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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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: 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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“…The actions of ER and GFs converge in a synergistic manner via a mechanism that is poorly understood. [17][18][19][20] ER activation can induce expression of other proteins that interact with and/or activate GFs, GF receptors, or GF signaling pathways. 21 Conversely, activation of intracellular kinases of the epidermal GF signal transduction pathway can phosphorylate ER and change its activity.…”

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confidence: 99%

Estrogen Stimulates Delayed Mitogen-Activated Protein Kinase Activity in Human Endothelial Cells via an Autocrine Loop That Involves Basic Fibroblast Growth Factor

Kim‐Schulze

Lowe

1998

Circulation

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Background-Estrogen plays a significant role in protecting premenopausal women from cardiovascular disease. We have found that estradiol augments endothelial cell activities related to vascular healing and that human coronary artery and umbilical vein endothelial cells express estrogen receptors (ERs). Classically, the ER functions as a transcription factor, but the cytoplasmic targets of this genomic effect have not been defined for endothelial cells. In the present study, we examined the potential role of the mitogen-activated protein (MAP) kinases ERK1 and ERK2 as mediators of estrogen action. Methods and Results-Human umbilical vein endothelial cells were estrogen depleted by culturing in hormone-free medium for 48 hours before experiments. 17␤-Estradiol (E2) stimulated a delayed (3 hours) 5-to 7-fold induction of ERK1/2 activity requiring activation of ER and new transcription/translation. Conditioned media from cells stimulated for 3 hours with E2 induced immediate ERK1/2 activation and phosphorylation of the basic fibroblast growth factor (bFGF) receptor. Moreover, ERK1/2 activation by E2 or by conditioned media was abrogated by treatment with neutralizing anti-bFGF antibody. Conclusions-These data describe an autocrine mechanism for E2 induction of ERK1/2 in HUVEC. Because our previous studies suggested that certain cardioprotective effects of estrogen are genomic in nature, the results are consistent with the hypothesis that autocrine stimulation of endothelial ERK1/2 activity by bFGF may play a role in the beneficial effects of estrogen on cardiovascular biology. (Circulation. 1998;98:413-421.)

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“…In our previous study in which ENU was intraperitoneally injected into heterozygous p53 deficient mice of the CBA strain [p53(+/-) mice], the incidences of endometrial stromal sarcomas and atypical hyperplasias of the endometrial glands were significantly increased in p53(+/-) mice as compared to their wild littermates [p53(+/+) mice] 18 . As the potential mechanism on the enhancement of uterine carcinogenesis of estrogen, it is well known that chemicals with estrogenic activity typically bind the estrogen response elements (ERE), and that transcription factors are recruited to the estrogen receptor-ligand/ERE complex, resulting in enhanced mRNA synthesis and gene expression of polypeptide growth factors such as epidermal growth factor (EGF) and transforming growth factor (TGF)-β , which can stimulate cell proliferation [31][32][33] . With regard to the carcinogenicity, ATR at a dose of 750 ppm induced mammary carcinomas and uterine endometrial adenocarcinomas in F344 rats over 24 months 12 .…”

Section: Discussionmentioning

confidence: 99%

Promoting Effects of Ethinylestradiol but not Atrazine on <i>N</i>-ethyl-<i>N</i>-nitrosourea-induced Uterine Carcinogenesis in ICR Mice

et al. 2003

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Abstract:In order to assess the modifying effects of atrazine (ATR) on uterine endometrial carcinogenesis, female ICR mice received an intra-uterine injection via the vagina of 50 mg/kg body weight of N-ethyl-N-nitrosourea (ENU), followed by no further treatment, by a diet containing 5, 50 or 500 ppm ATR or by a diet containing 2.5 ppm ethinylestradiol (EE) for 26 weeks. In the ENU + EE (positive control) group, depression of body weight gain was seen throughout the treatment period, and the incidence of uterine endometrial proliferative lesions such as adenocarcinomas and atypical hyperplasias, and PCNA positive indices were significantly increased as compared to the ENU alone group. On the other hand, although only slight depression of body weight was seen throughout the study in the ENU + 500 ppm ATR group, but no significant differences in uterine weights, incidence of uterine proliferative lesions with their PCNA positive indices and the immunohistochemical expression of ERα were found in all of the ENU + ATR groups as compared with those of the ENU alone group. The results in the present study indicate that ATR up to 500 ppm in diet has no modifying effects on uterine carcinogenesis in ICR mice initiated with ENU. (J Toxicol Pathol 2003; 16: 139-145)

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Regulation of uterine epidermal growth factor (EGF) receptors by estrogen in the mature rat and during the estrous cycle

Cited by 82 publications

References 17 publications

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

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

Estrogen Stimulates Delayed Mitogen-Activated Protein Kinase Activity in Human Endothelial Cells via an Autocrine Loop That Involves Basic Fibroblast Growth Factor

Promoting Effects of Ethinylestradiol but not Atrazine on <i>N</i>-ethyl-<i>N</i>-nitrosourea-induced Uterine Carcinogenesis in ICR Mice

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