Hormonal regulation and localization of estrogen, progestin and androgen receptors in the endometrium of nonhuman primates: effects of progesterone receptor antagonists

Ov D Slayden, Robert Brenner, Robert M Brenner
Archives of histology and cytology · 2004 · vol. 67(5) , pp. 393–409 · doi:10.1679/aohc.67.393 · PMID:15781981 · W1977213650
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⚙ AI-generated summary by claude@2026-06, 2026-06-09 ⓘ

Estradiol upregulates estrogen, progesterone, and androgen receptors in the primate endometrium, while progesterone induces secretory differentiation and receptor suppression, and progesterone antagonists block these effects and inhibit estrogen-dependent endometrial proliferation.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-09 · read from full text ⓘ

This review article analyzes how estradiol, progesterone, and progesterone receptor (PR) antagonists regulate and localize estrogen, progestin, and androgen receptors in the endometrium of ovariectomized rhesus macaques treated with precisely controlled hormone implants. It reports that estradiol alone induces a proliferative phase with increased stromal and epithelial estrogen receptor (ER) and PR expression, while androgen receptor (AR) is upregulated by estradiol and expressed in the endometrial stroma; progesterone then drives secretory differentiation and suppresses ER/PR (epithelium and stroma) and stromal AR in the functionalis zone, with epithelial ER and PR retained in the basalis zone during the secretory phase. Acute PR antagonism at the end of an E2+P cycle triggers menses resembling progesterone withdrawal, whereas chronic PR antagonism blocks both progesterone-dependent effects (including ER/PR/AR upregulation and glandular secretory function) and also inhibits estrogen-dependent endometrial proliferation and growth; the review is based on nonhuman primate experimental models and synthesized findings rather than new experimental data. This paper is centrally about adenomyosis/endometriosis-relevant mechanisms—specifically, it cites progesterone receptor antagonists and links their antiproliferative action to clinical use for controlling endometriosis, even though it focuses on rhesus macaque endometrial receptor regulation.

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Abstract

This article reviews the effects of estradiol (E(2)), progesterone (P) and P receptor antagonists (PA) on the rhesus macaque endometrium. Ovariectomized macaques can be treated with implants of estradiol (E(2)) and P to induce precisely controlled, artificial menstrual cycles. During these cycles, treatment with E(2) alone induces an artificial proliferative phase marked by extensive endometrial epithelial cell proliferation and increased expression of stromal and epithelial estrogen receptor (ER) and P receptor (PR). Androgen receptor (AR) is also upregulated by E(2) but is expressed only by the endometrial stroma. Progesterone acts on the E(2) primed endometrium to induce secretory differentiation and causes suppression of epithelial and stromal ER, epithelial PR, and stromal AR in the functionalis zone. However, epithelial ER and PR are retained in the basalis zone during the secretory phase. When potent P antagonists (PA) are administered acutely at the end of an E(2) + P induced cycle, menses typically ensues similar to P withdrawal at the end of the menstrual cycle. When PAs are administered chronically there is significant blockage of all P- dependent effects including upregulation of ER, PR and AR and suppression of glandular secretory function. However, chronic PA administration also inhibits estrogen-dependent endometrial cell proliferation and growth. This endometrial antiproliferative effect is the basis of the clinical use of PA to control various diseases such as endometriosis.
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Review articles Hormonal regulation and localization of estrogen, progestin and androgen receptors in the endometrium of nonhuman primates: effects of progesterone receptor antagonists 2004 Volume 67 Issue 5 Pages 393-409 Details Abstract This article reviews the effects of estradiol (E2), progesterone (P) and P receptor antagonists (PA) on the rhesus macaque endometrium. Ovariectomized macaques can be treated with implants of estradiol (E2) and P to induce precisely controlled, artificial menstrual cycles. During these cycles, treatment with E2 alone induces an artificial proliferative phase marked by extensive endometrial epithelial cell proliferation and increased expression of stromal and epithelial estrogen receptor (ER) and P receptor (PR). Androgen receptor (AR) is also upregulated by E2 but is expressed only by the endometrial stroma. Progesterone acts on the E2 primed endometrium to induce secretory differentiation and causes suppression of epithelial and stromal ER, epithelial PR, and stromal AR in the functionalis zone. However, epithelial ER and PR are retained in the basalis zone during the secretory phase. When potent P antagonists (PA) are administered acutely at the end of an E2+P induced cycle, menses typically ensues similar to P withdrawal at the end of the menstrual cycle. When PAs are administered chronically there is significant blockage of all P- dependent effects including upregulation of ER, PR and AR and suppression of glandular secretory function. However, chronic PA administration also inhibits estrogen-dependent endometrial cell proliferation and growth. This endometrial antiproliferative effect is the basis of the clinical use of PA to control various diseases such as endometriosis. © 2004 by International Society of Histology and Cytology Favorites & Alerts Recently viewed articles Predecessor

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Condition tags

endometriosis

MeSH descriptors

Endometrium Endometrium Macaca mulatta Progesterone Receptors, Androgen Receptors, Estrogen Receptors, Progesterone Animals Cell Proliferation Cell Proliferation Drug Implants Drug Synergism Endometrium Epithelial Cells Epithelial Cells Estradiol Estradiol Female Humans Macaca mulatta

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