# The role of ARID1A in endometriosis-related infertility

> **NIH NIH F31** · MICHIGAN STATE UNIVERSITY · 2021 · $30,356

## Abstract

ABSTRACT
Endometriosis occurs when endometrial tissue grows outside the uterine cavity, and this painful disease afflicts
about 10% of reproductive-aged women. Up to 50% of these women also experience infertility, and many
cases cannot be explained by morphological or ovarian defects, which implicates a uterine environment non-
receptive to embryo implantation. The molecular basis for the correlation of endometriosis and uterine non-
receptivity is unclear, but it likely involves signaling downstream of the steroid hormones progesterone and
estrogen in the endometrium. Progesterone and estrogen signaling must be tightly regulated for the successful
establishment and maintenance of pregnancy but they imbalanced in endometriosis, leading to progesterone
resistance and estrogen dominance. ARID1A, a chromatin remodeling factor, is directly associated with
progesterone signaling through the progesterone receptor and is remarkably reduced in the endometrium of
infertile women with endometriosis. ARID1A is necessary for fertility in mice due to its role supporting
implantation, decidualization, and endometrial receptivity. Uterine loss of ARID1A results in aberrant epithelial
proliferation characteristic of progesterone resistance in women with endometriosis. We hypothesize that
ARID1A loss provides the molecular key to endometriosis-related infertility by causing increased endometriotic
lesion development and decreased endometrial receptivity based on its role regulating steroid hormone
signaling. We will address the complex problem of endometriosis-related infertility by examining the causal link
between ARID1A loss in endometriotic lesions and the development of endometriosis-related infertility (Aim 1)
as well as the endometrial compartment-specific role of ARID1A loss in the dysregulation of steroid hormone
signaling observed in the eutopic endometrium of women endometriosis (Aim 2). Our innovative endometriosis
model mice, uterine Arid1a knockout mice, and tissue samples from infertile women with endometriosis will be
powerful tools to analyze ARID1A's role in the pathophysiology of endometriosis-related infertility and the
dysregulated molecular mechanisms of steroid hormone signaling in the endometriosis-affected uterus.

## Key facts

- **NIH application ID:** 10216183
- **Project number:** 5F31HD101207-02
- **Recipient organization:** MICHIGAN STATE UNIVERSITY
- **Principal Investigator:** Ryan Marquardt
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $30,356
- **Award type:** 5
- **Project period:** 2020-08-16 → 2022-05-15

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10216183

## Citation

> US National Institutes of Health, RePORTER application 10216183, The role of ARID1A in endometriosis-related infertility (5F31HD101207-02). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10216183. Licensed CC0.

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