Endometrial epithelial ARID1A is critical for uterine gland function in early pregnancy establishment

Ryan M. Marquardt, Tae Hoon Kim, Jung‐Yoon Yoo, Hanna E. Teasley, Fazleabas AT, Asgerally T Fazleabas, Steven L. Young, Bruce A. Lessey, Lessey BA, Ripla Arora, Jae‐Wook Jeong
FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020 · vol. 35(2) , pp. e21209 · doi:10.1096/fj.202002178r · PMID:33222288 · PMC8076973 · W3109422515
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ARID1A in mouse endometrial epithelium is critical for uterine gland function and early pregnancy establishment by regulating FOXA2 and LIF expression, and its loss correlates with endometriosis in women and nonhuman primates.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-12 · read from full text ⓘ

This study investigated the role of ARID1A in uterine/endometrial epithelial cells for early pregnancy establishment, using mouse models with uterine-specific or adult endometrial epithelial deletion of Arid1a and assessing gland development, receptivity, implantation, and downstream gene expression. The authors found that ARID1A binds and regulates Foxa2, and that Arid1a loss impairs uterine gland development and reduces Foxa2 and Lif, while adult epithelial deletion preserves gland development but still compromises gland function and disrupts implantation/decidualization through the LIF–STAT3–EGR1 pathway. A key caveat is that mechanistic conclusions rely on genetic mouse models and associated expression correlations rather than direct demonstration of ARID1A-driven causality for all observed fertility defects in humans. Relevance to endometriosis: the paper links its ARID1A findings to endometriosis-related endometrial non-receptivity and reports reduced ARID1A/FOXA2 in women with endometriosis and in endometriosis-induced nonhuman primates, making it directly relevant to endometriosis mechanisms and potential targets. This paper is centrally about endometriosis — it focuses on ARID1A-mediated endometrial epithelial regulation of gland function that relates to endometriosis-associated endometrial non-receptivity and infertility.

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Abstract

Though endometriosis and infertility are clearly associated, the pathophysiological mechanism remains unclear. Previous work has linked endometrial ARID1A loss to endometriosis-related endometrial non-receptivity. Here, we show in mice that ARID1A binds and regulates transcription of the Foxa2 gene required for endometrial gland function. Uterine-specific deletion of Arid1a compromises gland development and diminishes Foxa2 and Lif expression. Deletion of Arid1a with Ltf-iCre in the adult mouse endometrial epithelium preserves the gland development while still compromising the gland function. Mice lacking endometrial epithelial Arid1a are severely sub-fertile due to defects in implantation, decidualization, and endometrial receptivity from disruption of the LIF-STAT3-EGR1 pathway. FOXA2 is also reduced in the endometrium of women with endometriosis in correlation with diminished ARID1A, and both ARID1A and FOXA2 are reduced in nonhuman primates induced with endometriosis. Our findings describe a role for ARID1A in the endometrial epithelium supporting early pregnancy establishment through the maintenance of gland function.
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YUHASpace Repository 0 538 Cited 0 times in Cited 21 times in Endometrial epithelial ARID1A is critical for uterine gland function in early pregnancy establishment - Authors - Ryan M Marquardt ; Tae Hoon Kim ; Jung-Yoon Yoo ; Hanna E Teasley ; Asgerally T Fazleabas ; Steven L Young ; Bruce A Lessey ; Ripla Arora ; Jae-Wook Jeong - Citation - FASEB JOURNAL, Vol.35(2) : e21209, 2021-02 - Journal Title - FASEB JOURNAL - ISSN - 0892-6638 - Issue Date - 2021-02 - MeSH - Adult ; Animals ; DNA-Binding Proteins / genetics ; DNA-Binding Proteins / metabolism* ; Embryo Implantation* ; Endometrium / metabolism* ; Female ; Hepatocyte Nuclear Factor 3-beta / genetics ; Hepatocyte Nuclear Factor 3-beta / metabolism ; Humans ; Leukemia Inhibitory Factor / genetics ; Leukemia Inhibitory Factor / metabolism ; Mice ; Mice, Inbred C57BL ; Pregnancy ; Transcription Factors / genetics ; Transcription Factors / metabolism* - Keywords - ARID1A ; FOXA2 ; endometriosis ; endometrium ; infertility - Abstract - Though endometriosis and infertility are clearly associated, the pathophysiological mechanism remains unclear. Previous work has linked endometrial ARID1A loss to endometriosis-related endometrial non-receptivity. Here, we show in mice that ARID1A binds and regulates transcription of the Foxa2 gene required for endometrial gland function. Uterine-specific deletion of Arid1a compromises gland development and diminishes Foxa2 and Lif expression. Deletion of Arid1a with Ltf-iCre in the adult mouse endometrial epithelium preserves the gland development while still compromising the gland function. Mice lacking endometrial epithelial Arid1a are severely sub-fertile due to defects in implantation, decidualization, and endometrial receptivity from disruption of the LIF-STAT3-EGR1 pathway. FOXA2 is also reduced in the endometrium of women with endometriosis in correlation with diminished ARID1A, and both ARID1A and FOXA2 are reduced in nonhuman primates induced with endometriosis. Our findings describe a role for ARID1A in the endometrial epithelium supporting early pregnancy establishment through the maintenance of gland function. - Appears in Collections: - 1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers - Yonsei Authors - Yoo, Jung Yoon(유정윤) https://orcid.org/0000-0001-9366-3863 Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

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Condition tags

endometriosisinfertility

MeSH descriptors

DNA-Binding Proteins Embryo Implantation Endometrium Transcription Factors Adult Animals DNA-Binding Proteins DNA-Binding Proteins Endometrium Female Hepatocyte Nuclear Factor 3-beta Hepatocyte Nuclear Factor 3-beta Hepatocyte Nuclear Factor 3-beta Humans Leukemia Inhibitory Factor Leukemia Inhibitory Factor Leukemia Inhibitory Factor Mice Mice, Inbred C57BL Pregnancy

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