Increased FOXL2 Expression Alters Uterine Structures and Functions

Rong Li, San‐Pin Wu, Lecong Zhou, Barbara Nicol, John P. Lydon, Humphrey Hung‐Chang Yao, Francesco J. DeMayo
In: bioRxiv · 2020 · doi:10.1101/2020.03.06.981266 · W3010512042
preprint OA: green CC0 ⤵ 1 in-corpus citation
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Overexpression of FOXL2 in female mice disrupts uterine morphology, function, and fertility, and its transcriptome correlates with human endometriosis endometrium.

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Abstract

Abstract Transcription factor FOXL2 exhibits an increase in mRNA levels in eutopic endometrial biopsy in endometriosis patients. While FOXL2 is known of regulating sex differentiation and reproductive function, the impact of elevated FOXL2 expression on uterine physiology remains unknown. To answer this question, we generated mice with over expression of FOXL2 (FOXL2 OE ) in the female reproductive tract by crossing Foxl2 LsL/+ with the Pgr cre model. FOXL2 OE uterus showed severe morphological abnormality including abnormal epithelial stratification, blunted adenogenesis, increased endometrial fibrosis and disrupted myometrial morphology. In contrast, increasing FOXL2 levels specifically in uterine epithelium by crossing the Foxl2 LsL/+ with the Ltf icre mice resulted in the eFOXL2 OE mice with uterine epithelial stratification but without defects in endometrial fibrosis and adenogenesis, demonstrating a role of the endometrial stroma in the uterine abnormalities of the FOXL2 OE mice. Transcriptomic analysis of 12 weeks old Pgr cre and FOXL2 OE uterus at diestrus stage showed a positive correlation of FOXL2 OE uterine transcriptome with human endometrium of endometriosis patients. Furthermore, we found FOXL2 OE mice were sterile. The infertility was caused in part by a disruption of the hypophyseal ovarian axis resulting in an anovulatory phenotype. The FOXL2 OE mice failed to show decidual responses during artificial decidualization in ovariectomized mice which demonstrates the uterine contribution to the infertility phenotype. These data supported that aberrantly increased FOXL2 expressions in the female reproductive tract can disrupt ovarian and uterine functions, particularly, may be involved in the progressions of endometriosis.

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endometriosisinfertility

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