17β-HSD type 5 expression and the emergence of differentiated epithelial Type II cells in fetal lung: A novel role for androgen during the surge of surfactant
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Abstract
Lung maturation is delayed in male fetuses compared to female fetuses. This has been
attributed to higher levels of androgens in the male lung. We previously showed that
the genes encoding for the 17beta-hydroxysteroid dehydrogenase (HSD) type 5 (conversion
of androstenedione in testosterone) and type 2 (the opposite reaction) are, respectively,
expressed in the human epithelial Type II (PTII)-like A549 cells and in human lung
fibroblasts. Here, we aim to explain the physiological relevance of androgen synthesis
by PTII cells. We showed that 17beta-HSD type 2 and type 5 genes are both up-regulated
in correlation with the emergence of mature PTII cells in both male and female developing
lungs of the fetal mouse. In contrast, the androgen receptor gene is expressed at
similar levels in both sexes with no temporal regulation. In conclusion, the expression
profile of the 17beta-HSD type 5 gene does not explain the presence of higher levels
of androgens in the male fetal lung but that androgen synthesis must be a normal characteristic
of mature PTII cells for both sexes. The production of androgens after the emergence
of mature PTII cells should negatively regulate PTII cell maturation and thus, a novel
and normal role for androgens in cell reprogramming is proposed.