Human type 2 17beta-hydroxysteroid dehydrogenase in umbilical vein and artery endothelial cells: differential inactivation of sex steroids according to the vessel type.

The human placenta produces high amounts of estradiol. 17β-hydroxysteroid dehydrogenase type 2 (17βHSD2) is expressed by placental endothelial cells and was proposed to regulate sex hormone levels. Previous results obtained in term placenta suggested that 17βHSD2 expression and activity differ among umbilical cord vessels. In this study, 17βHSD2 expression level and enzymatic activity, and estrogen receptor α and β expression levels, were measured in endothelial cell cultures from umbilical arteries (HUAEC) and vein (HUVEC) using real-time quantitative PCR, western blot, and radiolabeled steroids. 17βHSD2-specific activities were also measured in proximal and distal segments of freshly isolated umbilical cord arteries and vein. 17βHSD2 mRNA level and activity were higher in HUAEC than in HUVEC. Activity was higher in umbilical arteries than in the umbilical vein. In arteries, enzymatic activity was higher near the placenta, suggesting a gradient of expression. No difference was found in ERα expression, whereas ERβ was expressed at a higher level in HUAEC than in HUVEC. Expression profiles of estrogen receptors and 17βHSD2 suggest a vessel type-specific response to estrogens. Our data support a differential modulation of biologically active sex steroid levels according to the vessel type in the foeto-placental unit, with apparent higher inactivation in the arterial system.