Type 2 and 5 17beta-hydroxysteroid dehydrogenases and androgen receptor in human fetal lungs

Androgens delay fetal lung maturation through an androgen receptor (AR)-dependent mechanism. Type 2 and 5 17beta-hydroxysteroid dehydrogenases (17betaHSD) are involved in androgen inactivation and synthesis, respectively. We aimed to further characterize the human fetal lung potential for androgen m...

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Bibliographic Details
Published in:Molecular and cellular endocrinology 2010-05, Vol.319 (1-2), p.79-87
Main Authors: Simard, Marc, Plante, Julie, Boucher, Mélanie, Provost, Pierre R, Tremblay, Yves
Format: Article
Language:English
Subjects:
17-Hydroxysteroid Dehydrogenases - metabolism
Adult
Androgens - metabolism
Blotting, Western
Epithelial Cells - metabolism
Female
Fetus - metabolism
Humans
Immunohistochemistry
In Situ Hybridization
Lung - embryology
Lung - metabolism
Male
Pregnancy
Receptors, Androgen - metabolism
Reverse Transcriptase Polymerase Chain Reaction
RNA, Messenger - metabolism
Statistics, Nonparametric
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Summary:Androgens delay fetal lung maturation through an androgen receptor (AR)-dependent mechanism. Type 2 and 5 17beta-hydroxysteroid dehydrogenases (17betaHSD) are involved in androgen inactivation and synthesis, respectively. We aimed to further characterize the human fetal lung potential for androgen metabolism and response. 17betaHSD2, 17betaHSD5, and AR mRNA levels were determined in lungs of mid-late gestation and in adult lungs, while protein detections were performed at mid-gestation. Relationships between levels of each mRNA and gestational age were observed. AR protein levels showed important differences among individuals of the same gestational window. 17betaHSD2 and AR were co-localized in epithelial and mesenchymal cells. AR was detected in both, cytoplasm and nucleus, which suggests fine-tuning of AR occupancy. In contrast, 17betaHSD5 was localized in a few epithelial cells of conducting zones. Our results support the existence of a local androgen metabolism in male and female human fetal lungs during the period of high-risk premature birth.
ISSN:1872-8057
DOI:10.1016/j.mce.2009.12.007