| First Author | Hundertmark S | Year | 2002 |
| Journal | Horm Metab Res | Volume | 34 |
| Issue | 10 | Pages | 545-9 |
| PubMed ID | 12439781 | Mgi Jnum | J:80523 |
| Mgi Id | MGI:2446008 | Doi | 10.1055/s-2002-35425 |
| Citation | Hundertmark S, et al. (2002) Foetal lung maturation in 11beta-hydroxysteroid dehydrogenase type 1 knockout mice. Horm Metab Res 34(10):545-9 |
| abstractText | Glucocorticoids (GCs) induce surfactant synthesis in the late foetal lung. Deficient GC action causes respiratory distress syndrome (RDS). 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) converts inert cortisone (11-dehydrocorticosterone in rodents) into active cortisol (corticosterone), thus amplifying intracellular GC action. Reduction or loss of pulmonary 11beta-HSD1 activity in glycyrrhetinic acid-treated rats substantially impaired foetal lung maturation (Hundertmark et al., Horm Metab Res, this issue). To test these data, we investigated 11beta-HSD1 activity and lung maturity in the late foetal lung using 11beta-HSD1 knockout mice. Control foetal mice showed high 11beta-HSD activity in the late foetal lung and levels of plasma 11-dehydrocorticosterone were high. Lungs from 11beta-HSD1 -/- mice had lower surfactant protein-A (mRNA and protein) levels and significant depletion of lung surfactant according to both light and electron microscopy, and also had reduced amniotic fluid lecithin/sphingomyelin ratios. These results support the previous experiments with glycyrrhetinic acid and emphasize the importance of 11beta-HSD1 in foetal lung maturation. |
