11 beta-hydroxysteroid dehydrogenase type II and mineralocorticoid receptor in human placenta

Citation
G. Hirasawa et al., 11 beta-hydroxysteroid dehydrogenase type II and mineralocorticoid receptor in human placenta, J CLIN END, 85(3), 2000, pp. 1306-1309
Citations number
32
Categorie Soggetti
Endocrynology, Metabolism & Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM
ISSN journal
0021972X → ACNP
Volume
85
Issue
3
Year of publication
2000
Pages
1306 - 1309
Database
ISI
SICI code
0021-972X(200003)85:3<1306:1BDTIA>2.0.ZU;2-N
Abstract
In mineralocorticoid target organs, 11 beta-hydroxysteroid dehydrogenase ty pe II(11 beta-HSD2) confers specificity on the mineralocorticoid receptor ( MR) by converting biologically active glucocorticoids to inactive metabolit es. Placental 11 beta-HSD2 is also thought to protect the fetus from high l evels of circulating maternal glucocorticoid. In this study, we examined th e immunoreactivity of 11 beta-HSD2 and MR in human placenta from 5 weeks ge station to full term using immunohistochemistry, 11 beta-HSD2 messenger RNA (mRNA) expression using Northern blot analysis, and MR mRNA expression usi ng RT-PCR analysis. Marked 11 beta-HSD2 immunoreactivity was detected in pl acental syncytiotrophoblasts at all gestational stages. MR immunoreactivity was moderately detected in syncytiotrophoblasts, some cytotrophoblasts, an d interstitial cells of the villous core. Marked mRNA expression of 11 beta -RSD2 was detected in placenta by Northern analysis. RT-PCR analysis of MR in placental tissues showed an amplified product consistent in length with the primers selected. These results suggest that placental 11 beta-HSD2 is involved in not only regulating the passage of maternal active glucocortico ids into the fetal circulation but also in regulation of maternal-fetal ele ctrolyte and water transport in the placenta, as in other mineralocorticoid target organs.