Circadian rise in maternal glucocorticoid prevents pulmonary dysplasia in fetal mice with adrenal insufficiency

Citation
M. Venihaki et al., Circadian rise in maternal glucocorticoid prevents pulmonary dysplasia in fetal mice with adrenal insufficiency, P NAS US, 97(13), 2000, pp. 7336-7341
Citations number
42
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Multidisciplinary
Journal title
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
ISSN journal
0027-8424 → ACNP
Volume
97
Issue
13
Year of publication
2000
Pages
7336 - 7341
Database
ISI
SICI code
0027-8424(20000620)97:13<7336:CRIMGP>2.0.ZU;2-#
Abstract
The hypothalamic-pituitary-adrenal (HPA) axis, including hypothalamic corti cotropin-releasing hormone (CRH) and pituitary corticotropin, is one of the first endocrine systems to develop during fetal life, probably because glu cocorticoid secretion is necessary for the maturation of many essential fet al organs. Consistent with this. pregnant mice with an inactivating mutatio n in the Crh gene deliver CRH-deficient offspring that die at birth with dy splastic lungs, which can be prevented by prenatal maternal glucocorticoid treatment. But children lacking the ability to synthesize cortisol (because of various genetic defects in adrenal gland development or steroidogenesis ) are not born with respiratory insufficiency or abnormal lung development, suggesting that the transfer of maternal glucocorticoid across the placent a might promote fetal organ maturation in the absence of fetal glucocortico id production. We used pregnant mice with a normal HPA axis carrying fetuse s with CRH deficiency to characterize the relative contributions of the fet al and maternal adrenal to the activity of the fetal HPA axis, and related these findings to fetal lung development. We found that in the presence of fetal adrenal insufficiency, normal fetal lung development is maintained by the transfer of maternal glucocorticoid to the fetus, specifically during the circadian peak in maternal glucocorticoid secretion.