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A Link between Lung Androgen Metabolism and the Emergence of Mature Epithelial Type II Cells

Laboratory of Ontogeny and Reproduction, Department of Obstetrics and Gynecology, and Centre de Recherche en Biologie de la Reproduction, Faculty of Medicine, Laval University, Quebec, Quebec, Canada

Correspondence and reprint requests should be addressed to Dr. Yves Tremblay, Ph.D., Ontogeny and Reproduction, Room T-1-58, Centre Hospitalier Universitaire de Québec, Pavillon CHUL, 2705 Laurier Boul, G1V 4G2, Quebec, Quebec, Canada. E-mail: yves.tremblay{at}crchul.ulaval.ca

Lung maturation is delayed in male fetuses compared with 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 17ß-hydroxysteroid dehydrogenase (17ß-HSD) type 5 (androstenedione testosterone) and type 2 (the opposite reaction) are expressed in human epithelial type II (PTII)–like A549 cells and in human lung fibroblasts, respectively. Here, we aim to explain the physiological relevance of androgen synthesis by PTII cells. We showed that both 17ß-HSD type 2 and type 5 genes are upregulated 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 17ß-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: androgen receptor, 17ß-hydroxysteroid dehydrogenases • hyaline membrane disease • lung maturation • real-time polymerase chain reaction

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