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Related Experiment Video

Updated: Jun 13, 2025

Establishing 3D Endometrial Organoids from the Mouse Uterus
06:24

Establishing 3D Endometrial Organoids from the Mouse Uterus

Published on: January 6, 2023

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PCOS endometrium-derived epithelial organoids as a novel model to study endometrial dysfunction.

L Luyckx1,2, M Wei3, U Saarela1

  • 1Department of Obstetrics and Gynecology, Medical Research Centre, Research Unit of Clinical Medicine, Oulu University Hospital, University of Oulu, Oulu, Finland.

Human Reproduction (Oxford, England)
|June 11, 2025
PubMed
Summary

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Biomolecules·2026

Researchers established patient-derived endometrium epithelial organoids (EEOs) from women with PCOS, revealing increased inflammation and reduced receptivity. This novel model captures key endometrial abnormalities, offering insights into PCOS-related subfertility and pregnancy complications.

Area of Science:

  • Reproductive biology and endocrinology.
  • Organoid technology and in vitro modeling.
  • Genetics and molecular mechanisms of PCOS.

Background:

  • Endometrial dysfunction in Polycystic Ovary Syndrome (PCOS) contributes to subfertility and pregnancy complications.
  • Previous research on the PCOS endometrial epithelial compartment is limited.
  • No PCOS-derived endometrium epithelial organoids (EEOs) have been established previously.

Purpose of the Study:

  • To establish PCOS-derived EEOs from patient samples.
  • To investigate potential differences between PCOS EEOs and non-PCOS EEOs.
  • To utilize EEOs as a model for studying endometrial dysfunction in PCOS.

Main Methods:

  • EEOs were established from endometrial biopsies of women with PCOS (lean and overweight/obese) and BMI-matched controls.
Keywords:
dysfunctionepitheliumhuman endometriumorganoidspolycystic ovary syndrome

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Last Updated: Jun 13, 2025

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  • Organoids were cultured with steroid hormones and Wnt signaling inhibitors to simulate menstrual cycle phases, with/without androgen exposure.
  • Bulk RNA-sequencing, RT-qPCR, and morphological assessments (H&E, immunostaining) were used to analyze gene expression and morphology.

    • Main Results:

    • PCOS EEOs exhibited increased inflammation-related gene expression (OSMR, ICAM1) and reduced diameter compared to controls.
    • Overweight/obese PCOS EEOs showed aberrant steroid hormone response, with reduced expression of receptivity genes (PAEP, LIF).
    • Androgen exposure (DHT) did not significantly alter EEO transcriptome due to minimal androgen receptor expression.

    Conclusions:

    • Successfully established PCOS EEOs that recapitulate endometrial abnormalities, including inflammation and altered gene expression.
    • This novel organoid model provides a valuable tool for understanding PCOS-related endometrial dysfunction and its impact on fertility.
    • Findings suggest potential links between altered endometrial receptivity, inflammation, and increased pregnancy complications in PCOS.