miR-194-3p Represses the Progesterone Receptor and Decidualization in Eutopic Endometrium From Women With Endometriosis

Tianjiao Pei, Chang Liu, Tingting Liu, Li Xiao, Bin Luo, Jing Tan, Xueying Li, Guojun Zhou, Changling Duan, Chang-Ling Duan, Wei Huang
Endocrinology · 2018 · vol. 159(7) , pp. 2554–2562 · doi:10.1210/en.2018-00374 · PMID:29762665 · W2802728960
article OA: bronze CC0 ⤵ 47 in-corpus citations
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This study found that elevated miR-194-3p in eutopic endometrium from women with endometriosis represses progesterone receptor levels and impairs decidualization, contributing to progesterone resistance and reduced fertility.

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Abstract

Progesterone resistance in the eutopic endometrium (EuE) is suggested to be a critical factor for decreased endometrial receptivity and implantation failure in reproductive-aged women with endometriosis. Altered expression of miRNAs has been reported to play an important role in the pathophysiology of endometriosis-associated infertility. However, the underlying mechanisms of aberrant progesterone receptor (PR) and deficient decidualization regulated by miRNAs in endometriosis have not been thoroughly elucidated. The goal of this study was to explore the regulation and roles of miR-194-3p in aberrant PR expression and impaired decidualization in endometrial stromal cells (ESCs) from the EuE of women with mild or minimal endometriosis. Using a series of studies, we observed decreased PR mRNA expression and an increasing PR-A/PR-B mRNA ratio trend in the midsecretory phase of the EuE of women with minimal or mild endometriosis (n = 19) compared with controls (n = 14); the increased expression of miR-194-3p in the endometriosis group was consistent with previous microarray analysis. We also found that PR protein levels were inhibited by the transfection of ESCs with an miR-194-3p mimic and upregulated by miR-194-3p inhibition. As predicted by the bioinformatic analysis, the 3'-untranslated region luciferase assay indicated the direct regulation of PR expression by miR-194-3p. Furthermore, miR-194-3p overexpression inhibited the in vitro decidualization of ESCs via both cellular morphological changes and prolactin levels. Therefore, our study demonstrated that miR-194-3p contributes to progesterone resistance in endometriosis, which hinders fertility by repressing the levels of PR and decidualization in the EuE. Thus, miR-194-3p regulation is a future therapeutic strategy for endometriosis.

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Condition tags

mesh:D004715endometriosisinfertility

MeSH descriptors

Endometriosis MicroRNAs Receptors, Progesterone Adult Blotting, Western Cells, Cultured Endometriosis Endometriosis Female Humans MicroRNAs MicroRNAs Prolactin Prolactin Receptors, Progesterone Receptors, Progesterone RNA, Messenger RNA, Messenger Young Adult

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