11-BETA-HYDROXYSTEROID DEHYDROGENASE TYPE-2 IN HUMAN LUNG - POSSIBLE REGULATOR OF MINERALOCORTICOID ACTION

Citation
T. Suzuki et al., 11-BETA-HYDROXYSTEROID DEHYDROGENASE TYPE-2 IN HUMAN LUNG - POSSIBLE REGULATOR OF MINERALOCORTICOID ACTION, The Journal of clinical endocrinology and metabolism, 83(11), 1998, pp. 4022-4025
Citations number
30
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
0021972X
Volume
83
Issue
11
Year of publication
1998
Pages
4022 - 4025
Database
ISI
SICI code
0021-972X(1998)83:11<4022:1DTIHL>2.0.ZU;2-3
Abstract
11 beta-Hydroxysteroid dehydrogenase type 2 (11 beta HSD2) catalyzes t he conversion of cortisol to biologically inactive cortisone and is th ought to confer specificity on mineralocorticoid receptors (MR). Corti sol is a prerequisite for surfactant synthesis and fetal lung maturati on. Recently, expression of 11 beta HSD2 was demonstrated in human fet al lung, but its localization and possible biological roles remain unk nown. Therefore, in this study, we examined immunohistochemical locali zation of 11 beta HSD2, MR, and glucocorticoid receptor (GR) in nonpat hological human lungs from fetus to adult (8 weeks gestation to 55 yr of age; n = 40) retrieved om pathology files. Both 11 beta HSD2 and MR immunoreactivities were detected in airway epithelia, from bronchiole to trachea and in fetal and neonatal ciliated collecting duct cells o f tracheal and bronchial glands, but were undetectable in alveoli. On the other hand, GR was detected in all cell types. These results indic ate that 11 beta HSD2 colocalizes with MR in human airway epithelia an d suggest that 11 beta HSD2 play an important role in pulmonary minera locorticoid activity such as sodium and fluid transport.