Laboratory of Ontogeny and Reproduction, Centre de Recherche du Centre Hospitalier de l'Université Laval (CHUL), Centre Hospitalier Universitaire de Québec (CHUQ), Canada.
Mol Cell Endocrinol. 2010 May 5;319(1-2):79-87. doi: 10.1016/j.mce.2009.12.007. Epub 2009 Dec 16.
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.
雄激素通过雄激素受体（AR）依赖性机制延迟胎儿肺成熟。2 型和 5 型 17β-羟类固醇脱氢酶（17βHSD）分别参与雄激素失活和合成。我们旨在进一步描述人胎儿肺对雄激素代谢和反应的潜力。在中晚期妊娠和成人肺中测定了 17βHSD2、17βHSD5 和 AR mRNA 水平，而在妊娠中期进行了蛋白质检测。观察了每种 mRNA 水平与胎龄之间的关系。在同一胎龄窗的个体中，AR 蛋白水平存在显著差异。17βHSD2 和 AR 均在上皮细胞和间充质细胞中存在共定位。AR 存在于细胞质和细胞核中，这表明 AR 占据的精细调节。相比之下，17βHSD5 仅存在于导气区的少数上皮细胞中。我们的研究结果支持在高风险早产期间，男性和女性胎儿肺中存在局部雄激素代谢。
