11-beta-hydroxysteroid dehydrogenase type 2

Definition:

Catalyzes the conversion of biologically active 11beta-hydroxyglucocorticoids (11beta-hydroxysteroid) such as cortisol, to inactive 11-ketoglucocorticoids (11-oxosteroid) such as cortisone, in the presence of NAD(+). Functions as a dehydrogenase (oxidase), thereby decreasing the concentration of active glucocorticoids, thus protecting the nonselective mineralocorticoid receptor from occupation by glucocorticoids. Plays an important role in maintaining glucocorticoids balance during preimplantation and protects the fetus from excessive maternal corticosterone exposure (By similarity). Catalyzes the oxidation of 11beta-hydroxytestosterone (11beta,17beta-dihydroxyandrost-4-ene-3-one) to 11-ketotestosterone (17beta-hydroxyandrost-4-ene-3,11-dione), a major bioactive androgen. Catalyzes the conversion of 11beta-hydroxyandrostenedione (11beta-hydroxyandrost-4-ene-3,17-dione) to 11-ketoandrostenedione (androst-4-ene-3,11,17-trione), which can be further metabolized to 11-ketotestosterone. Converts 7-beta-25-dihydroxycholesterol to 7-oxo-25-hydroxycholesterol in vitro. 7-beta-25-dihydroxycholesterol (not 7-oxo-25-hydroxycholesterol) acts as ligand for the G-protein-coupled receptor (GPCR) Epstein-Barr virus-induced gene 2 (EBI2) and may thereby regulate immune cell migration. May protect ovulating oocytes and fertilizing spermatozoa from the adverse effects of cortisol (By similarity).

References:

[1]. Maria Tsachaki, et al. Absence of 11-keto reduction of cortisone and 11-ketotestosterone in the model organism zebrafish. J Endocrinol. 2017 Feb;232(2):323-335. [Content Brief]

[2]. A L Albiston, et al. Cloning and tissue distribution of the human 11 beta-hydroxysteroid dehydrogenase type 2 enzyme. Mol Cell Endocrinol. 1994 Nov;105(2):R11-7. [Content Brief]

[3]. Arne Meyer, et al. Species-specific differences in the inhibition of human and zebrafish 11β-hydroxysteroid dehydrogenase 2 by thiram and organotins. Toxicology. 2012 Nov 15;301(1-3):72-8. [Content Brief]

[4]. Silvia G Inderbinen, et al. Species-specific differences in the inhibition of 11β-hydroxysteroid dehydrogenase 2 by itraconazole and posaconazole. Toxicol Appl Pharmacol. 2021 Feb 1;412:115387. [Content Brief]

[5]. P M Stewart, et al. Hypertension in the syndrome of apparent mineralocorticoid excess due to mutation of the 11 beta-hydroxysteroid dehydrogenase type 2 gene. Lancet. 1996 Jan 13;347(8994):88-91. [Content Brief]

[6]. Atanas G Atanasov, et al. Impaired protein stability of 11beta-hydroxysteroid dehydrogenase type 2: a novel mechanism of apparent mineralocorticoid excess. J Am Soc Nephrol. 2007 Apr;18(4):1262-70. [Content Brief]

[7]. A Odermatt, et al. The N-terminal anchor sequences of 11beta-hydroxysteroid dehydrogenases determine their orientation in the endoplasmic reticulum membrane. J Biol Chem. 1999 Oct 1;274(40):28762-70. [Content Brief]

[8]. Cristian A Carvajal, et al. Two homozygous mutations in the 11 beta-hydroxysteroid dehydrogenase type 2 gene in a case of apparent mineralocorticoid excess. J Clin Endocrinol Metab. 2003 Jun;88(6):2501-7. [Content Brief]

[9]. Katharina R Beck, et al. Enzymatic interconversion of the oxysterols 7β,25-dihydroxycholesterol and 7-keto,25-hydroxycholesterol by 11β-hydroxysteroid dehydrogenase type 1 and 2. J Steroid Biochem Mol Biol. 2019 Jun;190:19-28. [Content Brief]

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