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Endocrinology Vol. 144, No. 6 2534-2545
Copyright © 2003 by The Endocrine Society

11ß-Hydroxysteroid Dehydrogenase Complementary Deoxyribonucleic Acid in Rainbow Trout: Cloning, Sites of Expression, and Seasonal Changes in Gonads

Makoto Kusakabe, Ikumi Nakamura and Graham Young

Department of Zoology, University of Otago (M.K., I.N., G.Y.), Dunedin 9001, New Zealand; Department of Biological Sciences and Center for Reproductive Biology, University of Idaho (G.Y.), Moscow, Idaho 83844

Address all correspondence and requests for reprints to: Dr. Graham Young, Department of Biological Sciences and Center for Reproductive Biology, University of Idaho, P.O. Box 443051, Moscow, Idaho 83844-3051. E-mail: gyoung{at}uidaho.edu.

11ß-Hydroxysteroid dehydrogenases (11ß-HSDs) are important steroidogenic enzymes for catalyzing the interconversion of active glucocorticoid (cortisol and corticosterone) and inert 11-keto forms (cortisone and 11-dehydrocorticosterone) in mammals. In teleosts, 11ß-HSD also plays a role in the production of the predominant androgen, 11-ketotestosterone, in male fish. In this study we cloned cDNAs encoding rainbow trout 11ß-HSD (rt11ß-HSD) from testes and head kidney. The predicted amino acid sequence, hydrophobicity analysis, and transient transfection assays with rt11ß-HSD in HEK293 cells showed that rt11ß-HSD is a homolog of mammalian 11ß-HSD type 2. rt11ß-HSD transcripts are present in steroidogenic tissues and in a number of other tissues. Strong in situ hybridization signals for rt11ß-HSD transcripts were found in Leydig cells of testes, in thecal cells of the early vitellogenic ovarian follicles, and in thecal and granulosa cells of the midvitellogenic and postovulatory follicles. Weaker signals were also found in head kidney interrenal cells from juvenile rainbow trout. Seasonal changes in rt11ß-HSD transcripts in testes showed a pattern similar to that of stress-induced serum cortisol levels, but not to serum androgen levels. High levels of rt11ß-HSD transcripts were found in ovarian follicles from late vitellogenesis through ovulation. These results raise the possibility of a role for rt11ß-HSD in the protection of developing gonads from the inhibitory effects of stress-induced cortisol.




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