Intact progesterone receptors are essential to counteract the proliferative effect of estradiol in a genetically engineered mouse model of endometriosis

Zongjuan Fang, Fang Z, Sijun Yang, Yang S, John P. Lydon, Lydon JP, Franco DeMayo, Francesco J. DeMayo, Tamura M, Mitsutoshi Tamura, Gurates B, Bilgin Gurates, Bilgin Gürateş, Bulun Se, Serdar E. Bulun
Fertility and sterility · 2004 · vol. 82(3) , pp. 673–678 · doi:10.1016/j.fertnstert.2004.01.048 · PMID:15374713 · W1990762437
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

Progesterone receptor deletion in a mouse model abrogated estradiol's proliferative effects on endometriosis-like lesions, highlighting the receptor's necessity in mediating hormone-driven tissue growth.

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Abstract

ObjectiveTo determine the role of P and its nuclear receptor PR in the growth of ectopic uterine tissue of mice with or without a disrupted PR gene.DesignAnimal study.SettingAcademic medical center.Animal(s)Female wild-type (WT) and transgenic knockout mice for P receptor (PRKO).Intervention(s)Endometriosis was induced in the following groups of ovariectomized adult mice: [1] untreated WT, [2] estradiol (E(2))-treated WT, [3] P-treated WT, [4] E(2) + P-treated WT, [5] untreated PRKO, [6] E(2)-treated PRKO, and [7] E(2) + P-treated PRKO (n = 5 in each group).Main outcome measure(s)The size of ectopic uterine tissue in WT and PRKO mice were compared between the groups subjected to treatments with P or E(2). Tissue proliferating cell nuclear antigen (PCNA) levels were compared among these groups.ResultsTreatment with P only significantly decreased the size of WT ectopic uterine tissue. The untreated PRKO ectopic uterine tissue was significantly larger than WT tissue. Estradiol increased the size of ectopic uterine tissues, and this E(2)-dependent growth could be suppressed by P in WT tissues but not in PRKO tissues. Finally, the hormone-dependent changes in ectopic uterine tissue size were accompanied by comparable alterations in PCNA levels.Conclusion(s)Intact PR in ectopic uterine tissue is essential to abolish E(2)-dependent or -independent proliferation. We also suggest that ectopic uterine tissue is associated with significantly increased resistance to P action and increased predisposition to E(2)-dependent proliferation in the absence of PR. Overall, these findings support the hypothesis that P resistance in human endometriosis may be due to the absence of sufficient levels of functional PR in this tissue.

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Condition tags

endometriosis

MeSH descriptors

Cell Division Endometriosis Estradiol Receptors, Progesterone Animals Cell Division Cell Division Disease Models, Animal Endometriosis Endometriosis Estradiol Female Mice Mice, Knockout Mice, Transgenic Receptors, Progesterone Receptors, Progesterone Receptors, Progesterone

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