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RESEARCH |
1 Department of Biochemistry and Molecular Biology, University College London, Gower Street, London WC1E 6BT, UK, 2 Institute of Zoology, Zoological Society of London, Regent’s Park, London NW1 4RY, UK, 3 Genus Plc, 3033 Nashville Road, Franklin, Kentucky 42135, USA, 4 Reproduction and Development Group, Department of Veterinary Basic Sciences, Royal Veterinary College, Royal College Street, London NW1 0TU, UK and 5 Division of Clinical Developmental Sciences, Academic Section of Obstetrics and Gynaecology, St George’s, University of London, Cranmer Terrace, Tooting SW17 0RE, UK
Correspondence should be addressed to A E Michael, Division of Clinical Developmental Sciences, Centre for Developmental and Endocrine Signalling, Academic Section of Obstetrics and Gynaecology, 3rd Floor, Lanesborough Wing, St George’s, University of London, Cranmer Terrace, London SW17 0RE, UK; Email: tony.michael{at}sgul.ac.uk
This study investigated cortisol inactivation by 11ß-hydroxysteroid dehydrogenase (11ß HSD) enzymes in porcine granulosa cells from antral follicles at different developmental stages and in ovarian cysts. In granulosa cells, cortisol oxidation increased threefold with antral follicle diameter (P < 0.001). This trend was paralleled by a threefold increase in NADP+-dependent 11ß-dehydrogenase activity in granulosa cell homogenates with follicle diameter. Intact granulosa cells from ovarian cysts exhibited significantly lower enzyme activities than cells from large antral follicles. Neither intact cells norcell homogenates displayed net 11-ketosteroid reductase activities. Since porcine follicular fluid (FF) from large antral follicles and ovarian cysts contains hydrophobic inhibitors of glucocorticoid metabolism by type 1 11ß HSD, this studyalso investigated whether levels of 11ß HSD inhibitors changed during follicle growth and could affect cortisol metabolism in granulosa cells. The extent of inhibition of 11ß HSD1 activity in rat kidney homogenates decreased progressively from 50 ± 8% inhibition by FF from small antral follicles (P < 0.001) to 23 ± 6% by large antral FF (P < 0.05). Cyst fluid inhibited 11ß HSD1 activity by 59 ± 4% (P < 0.001). Likewise, net cortisol oxidation in granulosa cells was significantly decreased by large antral FF (35–48% inhibition, P < 0.05) and cyst fluid (45–75% inhibition, P < 0.01). We conclude that inactivation of cortisol by 11ß HSD enzymes in porcine granulosa cells increases with follicle development but is significantly decreased in ovarian cysts. Moreover, changes in ovarian cortisol metabolism are accompanied by corresponding changes in the levels of paracrine inhibitors of 11ß HSD1 within growing ovarian follicles and cysts, implicating cortisol in follicle growth and cyst development.
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  C Chandras, T E Harris, A L. Bernal, D R E Abayasekara, and A E Michael PTGER1 and PTGER2 receptors mediate regulation of progesterone synthesis and type 1 11{beta}-hydroxysteroid dehydrogenase activity by prostaglandin E2 in human granulosa lutein cells J. Endocrinol., September 1, 2007; 194(3): 595 - 602. [Abstract] [Full Text] [PDF]
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 V. Sharp, L. M Thurston, R. C Fowkes, and A. E Michael 11{beta}-Hydroxysteroid dehydrogenase enzymes in the testis and male reproductive tract of the boar (Sus scrofa domestica) indicate local roles for glucocorticoids in male reproductive physiology Reproduction, September 1, 2007; 134(3): 473 - 482. [Abstract] [Full Text] [PDF]
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