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Glucocorticoid receptor-mediated regulation of MMP9 gene expression in human ovarian surface epithelial cells.

Abstract：

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.

journal_name

Fertil Steril

journal_title

Fertility and sterility

authors

Rae MT,Price D,Harlow CR,Critchley HO,Hillier SG

doi

10.1016/j.fertnstert.2008.06.040

subject

Has Abstract

pub_date

2009-08-01 00:00:00

pages

703-8

issue

2

eissn

0015-0282

issn

1556-5653

pii

S0015-0282(08)01387-3

journal_volume

92

pub_type

杂志文章

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