17-BETA-HYDROXYSTEROID-DEHYDROGENASE TYPE-1 AND TYPE-2 IN HUMAN PLACENTA - AN IMMUNOHISTOCHEMICAL STUDY WITH CORRELATION TO PLACENTAL DEVELOPMENT

In estrogen metabolism, the enzymatic properties of the 17 beta-hydrox ysteroid dehydrogenase (17 beta HSD) isozymes play very important role s in steroid hormone metabolism in various tissues, including the plac enta. 17 beta HSD type 1 catalyzes primarily the reduction of estrone (E-1) to estradiol (E-2), whereas 17 beta HSD type 2 catalyzes primari ly the oxidation of E-2 to E-1. In this study, we examined immunohisto chemical localization of 17 beta HSD types 1 and 2 in human placenta ( 31 cases) ranging from 4-40 weeks gestation. The immunoreactivity of 1 7 beta HSD type 1 was exclusively detected in syncytiotrophoblast from 4 weeks gestation to term placenta. Immunoreactivity of 17 beta HSD t ype 2 first appeared in endothelial cells of intravillous vessels at 1 2 weeks gestation, and the number of 17 beta HSD type 2-positive endot helial cells markedly increased up to 19 weeks, then reached a plateau . We quantitatively evaluated the 17 beta HSD type 2-positive endothel ial cells in chorionic villi and determined the ratio of 17 beta HSD t ype 2-positive endothelial cells using immunohistochemistry of CD34, a n endothelial antigen, in serial mirror tissue sections and subsequent image analysis using CAS 200. CD34 was detected from 4 weeks gestatio n, and its positive areas continued to increase toward term. The 17 be ta HSD type 2-positive area per CD34-positive area markedly increased from 13 weeks gestation and reached a plateau at 19 weeks gestation, i n which almost all endothelial cells were positive for 17 beta HSD typ e 2. 17 beta HSD type 2, therefore, is considered to prevent the passa ge of excessive estrogens into the fetal circulation at endothelial ce lls of the intravillous fetal capillaries by catalyzing the inactivati on of E-2 to E-1.