Published ahead of print on April 29, 2004, doi:10.1164/rccm.200312-1680OC
Am. J. Respir. Crit. Care Med., Volume 170, Number 3, August 2004, 296-305
A more recent version of this article appeared on August 1, 2004
Submitted on December 10, 2003
Accepted on April 28, 2004
A Link Between Lung Androgen Metabolism and the Emergence of Mature Epithelial Type II Cells
Pierre R Provost1, Marc Simard1, and Yves Tremblay2*
1 Laboratory of Ontogeny and Reproduction, Centre Hospitalier Universitaire de Quebec, Pavillion CHUL, Quebec, Quebec, Canada,
2 Laboratory of Ontogeny and Reproduction, Centre Hospitalier Universitaire de Quebec, Pavillion CHUL, Quebec, Quebec, Canada; Department of Ob/Gyn and Centre de Recherche en Biologie de la Reproduction (CRBR), Laval University, Quebec, Quebec, Canada
* To whom correspondence should be addressed. E-mail: marc-simard{at}crchul.ulaval.ca.
Lung maturation is delayed in male fetuses compared to female fetuses, which has been attributed to higher levels of androgens in the male lung. Our previous studies demonstrated that the genes encoding for the 17 -hydroxysteroid dehydrogenase (HSD) type 5 (androstenedione  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 both, 17-HSD type 2 and type 5 genes are up-regulated in correlation with the emergence of mature PTII cells in both male and female developing lungs of the mouse. In contrast, the androgen receptor gene is expressed equally in both sexes with no temporal regulation. We conclude that the expression profile of the 17-HSD type 5 gene does not explain the presence of higher levels of androgen in the male fetal lung but that androgen synthesis must be a normal feature 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 role for androgens in cell reprogramming is suggested.
Key words: 17-hydroxysteroid dehydrogenases, androgen receptor, lung maturation, hyaline membranne disease, real time PCR
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