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Updated: Jul 2, 2026
Human Ovarian Surface Epithelium Organoids as a Platform to Study Tissue Regeneration
Published on: August 16, 2024
Glucocorticoid receptor-mediated regulation of MMP9 gene expression in human ovarian surface epithelial cells
Michael T Rae1, Deborah Price, Christopher R Harlow
1Centre for Reproductive Biology, The Queen's Medical Research Institute, The University of Edinburgh, Edinburgh, United Kingdom.
Objective:
To obtain proof-of-concept that locally produced anti-inflammatory steroids suppress ovulation-associated extracellular matrix proteases in human ovarian surface epithelial (OSE) cells.
Design:
Primary OSE cell cultures treated with interleukin-1alpha (IL-1alpha) (500 pg/mL) as proxy for inflammation, with/without anti-inflammatory steroid (cortisol or progesterone [P], 0.01-1.0 microM).
Setting:
Academic medical center.
Patient(S):
Sixteen premenopausal women (29-46 years) undergoing surgery for nonmalignant gynecological conditions.
Main Outcome Measure(S):
Semiquantitative extracellular matrix protease gene expression profiling with verification by real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) and gelatinase zymography.
Result(S):
Treatment with IL-1alpha stimulated messenger RNA (mRNA) expression of several ovulation-associated matrix metalloproteinase genes by OSE cell cultures, including gelatinase B (MMP9) but not gelatinase A (MMP2). The IL-1alpha-stimulated MMP9 mRNA production was suppressed by cortisol but not P. Cortisol but not P also dose-dependently suppressed IL-1alpha-stimulated MMP9 gelatinase activity and this effect was blocked by the glucocorticoid receptor antagonist RU486.
Conclusion(S):
In human OSE cells, stimulation of MMP9 gene expression and proteolytic activity by IL-1alpha is suppressed by anti-inflammatory cortisol through a glucocorticoid receptor-mediated mechanism. Because IL-1alpha also generates cortisol formation in OSE by stimulating cortisone reductase activity, these results support a role for intracrine cortisol in minimizing proteolytic damage to the OSE at ovulation.
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