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

Oleh:

Rae, Michael T. ; Price, Deborah ; Harlow, Christopher R. ; Critchley, Hilary O.D.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Fertility and Sterility (keterangan: ada di ClinicalKey) vol. 92 no. 02 (Aug. 2009), page 703-708.
Topik: Ovarian surface epithelium; inflammation; ovulation; steroids; extracellular matrix; ovarian cancer

Ketersediaan

Perpustakaan FK Nomor Panggil: F02.K.2009.03 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

Lihat Detail Induk

Isi artikel

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-1a (IL-1a) (500 pg/mL) as proxy for inflammation, with/without anti-inflammatory steroid (cortisol or progesterone [P], 0.01–1.0 µM). 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-1a 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-1a-stimulated MMP9 mRNA production was suppressed by cortisol but not P. Cortisol but not P also dose-dependently suppressed IL-1a-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-1a is suppressed by anti-inflammatory cortisol through a glucocorticoid receptor-mediated mechanism. Because IL-1a 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.

Opini Anda

Klik untuk menuliskan opini Anda tentang koleksi ini!

Kembali