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Steroid signalling in the ovarian surface epithelium
Michael T Rae1, Stephen G Hillier
1Centre for Reproductive Biology, University of Edinburgh, The Chancellor's Building, 49 Little France Crescent, Edinburgh, United Kingdom EH16 4SB.
Trends in Endocrinology and Metabolism: TEM
|August 2, 2005
Summary
Ovarian surface epithelium (HOSE) cells activate anti-inflammatory cortisol during ovulation. This cortisol enhances its own production and action, offering insights into ovarian cancer and inflammation-associated reproductive diseases.
Area of Science:
- Reproductive biology
- Molecular endocrinology
- Oncology
Background:
- Human ovarian surface epithelium (HOSE) is prone to injury during ovulation, a process linked to ovarian epithelial cancers.
- Inflammation is implicated in ovarian cancer development, suggesting a role for anti-inflammatory steroid signaling in HOSE regulation.
Purpose of the Study:
- To investigate the role of steroid metabolism in HOSE regulation, particularly in response to ovulation-associated inflammation.
- To elucidate the mechanism of cortisol activation and its feedback regulation in HOSE cells.
Main Methods:
- In vitro analysis of HOSE cells.
- Gene expression studies for 11beta-hydroxysteroid dehydrogenase type 1 (HSD11B1) and glucocorticoid receptor.
- Assessment of cytokine-induced steroid metabolism.
Main Results:
- HOSE cells express hydroxysteroid dehydrogenase (HSD) enzymes for steroid precursor metabolism.
- Ovulation-associated cytokines up-regulate HSD11B1 in HOSE cells, converting cortisone to cortisol.
- Cortisol amplifies its own synthesis and action by enhancing HSD11B1 and glucocorticoid receptor gene expression.
Conclusions:
- A positive feed-forward loop exists where cortisol enhances its own formation and action in HOSE cells.
- This mechanism is crucial for regulating inflammation in HOSE and has implications for ovarian cancer and related reproductive diseases.