Deficiency of Immunophilin FKBP52 Promotes Endometriosis

Yasushi Hirota, Susanne Tranguch, Takiko Daikoku, Akiko Hasegawa, Hasegawa A, Osuga Y, Yutaka Osuga, Taketani Y, Yuji Taketani, Sudhansu K. Dey, Dey SK
The American Journal of Pathology · 2008 · vol. 173(6) , pp. 1747–1757 · doi:10.2353/ajpath.2008.080527 · PMID:18988805 · PMC2626386 · W2019014038
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Loss of FKBP52 in mice promotes endometriotic lesion growth with increased inflammation, proliferation, and angiogenesis, and FKBP52 is down-regulated in human endometriosis.

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Abstract

Endometriosis is a common gynecological disease that affects approximately 10% of women of childbearing age. It is characterized by endometrial growth outside the uterus and often results in inflamed lesions, pain, and reduced fertility. Although heightened estrogenic activity and/or reduced progesterone responsiveness are considered to be involved in the etiology of endometriosis, neither the extent of their participation nor the underlying mechanisms are clearly understood. Heterogeneous uterine cell types differentially respond to estrogen and progesterone (P(4)). P(4), primarily acting via its nuclear receptor (PR), activates gene transcription and impacts many reproductive processes. Deletion of Fkbp52, an immunophilin cochaperone for PR, results in uterine-specific P(4) resistance in mice, creating an opportunity to study the unique aspects of P(4) signaling in endometriosis. Here we explored the roles of FKBP52 in this disease using Fkbp52(-/-) mice. We found that the loss of FKBP52 encourages the growth of endometriotic lesions with increased inflammation, cell proliferation, and angiogenesis. We also found remarkable down-regulation of FKBP52 in cases of human endometriosis. Our results provide the first evidence corroborated by genetic studies in mice for a potential role of an immunophilin cochaperone in the etiology of human endometriosis. This investigation is highly relevant for clinical application, particularly because P(4) resistance is favorably indicated in endometriosis and other gynecological diseases.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Tacrolimus Binding Proteins Animals Cell Proliferation Chemokine CCL2 Chemokine CCL2 Chemokine CCL2 Cyclooxygenase 2 Cyclooxygenase 2 Disease Models, Animal Endometriosis Endometriosis Endometriosis Endometrium Endometrium Endometrium Estrogen Receptor alpha Estrogen Receptor alpha Estrogen Receptor alpha Female

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