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Adrenal 20-Hydroxysteroid Dehydrogenase in the Mouse Catabolizes Progesterone and 11-Deoxycorticosterone and Is Restricted to the X-Zone

Faculty of Health Sciences (L.H., M.K., Y.W.), Department of Microbiology and Immunology, Ben Gurion University of the Negev, Beer Sheva 84105, Israel; Division of Endocrinology and Diabetes (F.B., S.K.), Department of Internal Medicine II, University Hospital Freiburg, D-79104 Freiburg, Germany; and Medizinische Klinik-Innenstadt (F.B.), Ludwig-Maximilians-University, D-80336 Munich, Germany

Address all correspondence and requests for reprints to: Yacob Weinstein, Ph.D., Department of Microbiology and Immunology, Faculty of Health Sciences, Ben Gurion University of the Negev, Beer Sheva 84105, Israel. E-mail: yacob{at}bgu.ac.il.

The enzyme 20-hydroxysteroid dehydrogenase (20-HSD) is a progesterone-catabolizing enzyme that is highly expressed in mouse ovaries and adrenals. Although the functional significance of ovarian 20-HSD for the induction of parturition has been defined, regulation and distribution of 20-HSD in the adrenal gland has not been determined. We demonstrate that the expression of adrenal 20-HSD is restricted to the X-zone, a transient zone between the adrenal cortex and the medulla of yet unknown function. Adrenal 20-HSD activity in male mice peaks at 3 wk of age and disappears thereafter, whereas 20-HSD enzyme activity is maintained in adrenals from nulliparous female animals. Testosterone treatment of female mice induces rapid involution of the X-zone that is associated with the disappearance of the 20-HSD-positive cells. Conversely, reappearance of 20-HSD expression and activity in male animals is evident after gonadectomy. Moreover, pregnancy, but not pseudopregnancy, is accompanied by X-zone regression and loss of 20-HSD activity. Pregnancy-induced X-zone regression and -abolished 20-HSD expression is partially restored in animals that were kept from nursing their pups. We found that in addition to its progesterone-reducing activity, 20-HSD also functions as an 11-deoxycorticosterone-catabolizing enzyme. The unaltered growth kinetics of the X-zone in 20-HSD knockout animals suggests that 20-HSD is not required for the regulation of X-zone growth. However, 20-HSD expression and enzymatic activity in all experimental paradigms is closely correlated with the presence of the X-zone. These findings provide the basis for 20-HSD as a reliable marker of the murine X-zone.

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