REGULATION OF PROGESTERONE RECEPTOR FORMATION BY ESTROGEN ACTION<sup>*</sup>

Leavitt, Wendell W.; Chen, Tong J.; Allen, T. C.; Johnston, J.O'Neal

doi:10.1111/j.1749-6632.1977.tb29418.x

Cited by 184 publications

(46 citation statements)

References 11 publications

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“…synthesis of PRs and/or synthesis of polypeptide growth factors and other proteins (6). A decline in PR c was noted in both traumatized and non-traumatized uterine horns in our studies, presumably because of antagonism of estrogen action, since the synthesis is mainly regulated by estrogen (23,24). In this context it may be noted that clomiphene does not react with receptors but diminishes receptors, by one of the actions of estrogen on the uterus (6) and/or a disturbance in the balance of estrogen and progesterone as decidualization appears to be the result of estrogenic modulation and continual progesterone action.…”

Section: Discussionsupporting

confidence: 49%

Changes in uterine ornithine decarboxylase activity and steroid receptor levels during decidualization in the rat induced by CDRI-85/287

Dwivedi

Gupta

Keshri³

et al. 1999

European Journal of Endocrinology

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CDRI-85/287 is an anti-estrogen and interferes with decidualization in the rat uterus. In this study, uterine estrogen receptor (ER) and progesterone receptor (PR) levels were determined during the inhibition of decidualization. The effect of 85/287 on uterine ornithine decarboxylate (ODC) activity (a marker enzyme for decidualization) was also studied, using immature ovariectomized rats divided into four different groups: control, 2.5 mg/kg 85/287 only; 1 mg estradiol only; and 85/287 þ estradiol. Pseudopregnant rats were administered 85/287 (2.5 mg/kg p.o.) on day 3 post-coitum. Deciduoma was induced in one of the uterine horns on day 4 and animals were autopsied 18 h post-traumatization. Both ERs and PRs showed an increase in traumatized horns compared with non-traumatized. In the 85/287-treated uterus, there was a reduction in cytosolic ERs in both traumatized horns. However, nuclear ER and PR levels increased in both horns under the influence of 85/287. Similarly, in a tamoxifen (0.03 mg/kg)-treated group a decline was noticed in cytosolic ER with a mild increase in nuclear PR. Total ER content, expressed per 100 mg DNA, showed a decline in 85/287-or tamoxifentreated rats. However, no significant alterations were observed in total PR levels in non-traumatized horns. In an immature rat model, 85/287 caused a significant (> 50%) reduction in estradiol-induced ODC activity. These findings suggest that the decidualization inhibitory activity of 85/287 may be attributed to inhibition of certain timed biochemical events and genomic/non-genomic actions of estrogens in the rat uterus.

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Section: Discussionsupporting

confidence: 49%

Changes in uterine ornithine decarboxylase activity and steroid receptor levels during decidualization in the rat induced by CDRI-85/287

Dwivedi

Gupta

Keshri³

et al. 1999

European Journal of Endocrinology

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“…In this strain of rats, parturition usually occurs early in the afternoon of day 22. The rats (n ϭ 3-9 at each time point) were killed between 0900 and 1000 on day 13,15,16,18,19,21, or 22 of pregnancy, after delivery of the first pup (delivery), or on postpartum day 1. Rats were killed using an intraperitoneal injection of Euthanyl (100 mg/kg body wt).…”

Section: Methodsmentioning

confidence: 99%

“…Uterine PR may be regulated by estrogen and P 4 . Estrogen increases PR mRNA levels (12,14,15) and P 4 binding (16,17), whereas P 4 decreases the number of its own receptors (22,28). There is no information regarding the effect of estrogen or P 4 on the relative quantities of the PR isoforms in the late-pregnant uterus.…”

mentioning

confidence: 99%

Messenger RNA for progesterone receptor isoforms in the late-gestation rat uterus

Fang

Wong

Mitchell

2002

American Journal of Physiology-Endocrinology and Metabolism

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“…When PR was identified as an ERa-regulated gene, it was hypothesized that it would indicate an intact ER (Milgrom et al 1973, Leavitt et al 1977 and so predict the tumors that were more responsive to endocrine therapies (Horwitz & McGuire 1975). This has been supported by retrospective studies showing that patients whose tumors contain both the ERa and the PR have the greatest probability of responding to tamoxifen therapy and have a better prognosis than those whose tumors do not contain steroid receptors (Osborne et al 1980, Gross et al 1984, Ravdin et al 1992, Elledge et al 2000.…”

Section: Progesterone As a Downstream Targetmentioning

confidence: 99%

Pregnancy and the risk of breast cancer

Britt¹,

Ashworth²,

Smalley³

2007

Endocrine Related Cancer

196

175

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It is well established that childless women and women having children later in life are at an increased risk of developing breast cancer. In particular, women having a first child before 20 years of age have a 50% reduction in lifetime breast cancer risk when compared with women who do not have children. This protective effect is specific for estrogen receptor positive breast cancer. Nevertheless, it remains unclear how parity decreases breast cancer risk. Possible mechanisms of action include changes to the hormonal profile of parous women, a more differentiated and so less susceptible mammary gland or changes within specific epithelial cell subpopulations. In this review, we discuss the epidemiological evidence for the protective effects of parity on breast cancer. We also explore the mechanisms by which parity protects, with a particular emphasis on the role of stem cells and the interactions between stem cells and estrogen.

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REGULATION OF PROGESTERONE RECEPTOR FORMATION BY ESTROGEN ACTION^*

Cited by 184 publications

References 11 publications

Changes in uterine ornithine decarboxylase activity and steroid receptor levels during decidualization in the rat induced by CDRI-85/287

Changes in uterine ornithine decarboxylase activity and steroid receptor levels during decidualization in the rat induced by CDRI-85/287

Messenger RNA for progesterone receptor isoforms in the late-gestation rat uterus

Pregnancy and the risk of breast cancer

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REGULATION OF PROGESTERONE RECEPTOR FORMATION BY ESTROGEN ACTION*

Cited by 184 publications

References 11 publications

Changes in uterine ornithine decarboxylase activity and steroid receptor levels during decidualization in the rat induced by CDRI-85/287

Changes in uterine ornithine decarboxylase activity and steroid receptor levels during decidualization in the rat induced by CDRI-85/287

Messenger RNA for progesterone receptor isoforms in the late-gestation rat uterus

Pregnancy and the risk of breast cancer

Contact Info

Product

Resources

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REGULATION OF PROGESTERONE RECEPTOR FORMATION BY ESTROGEN ACTION^*