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17ß-Hydroxysteroid Dehydrogenase Types 1 and 2 in Human Placenta: An Immunohistochemical Study with Correlation to Placental Development¹

Department of Pathology (J.T., H.S., T.S., H.N.) and Pediatrics (J.T., K.I.), Tohoku University School of Medicine, Sendai, Japan; Cecil H. and Ida Green Center for Reproductive Biology Sciences, University of Texas Southwestern Medical Center (S.A.), Dallas, Texas 75235

Address all correspondence and requests for reprints to: Junji Takeyama, M.D., Department of Pathology, Tohoku University School of Medicine, 2–1 Seiryo-machi, Aoba-ku, Sendai 980-8575, Japan. E-mail: j-takeyama{at}patholo2.med.tohoku.ac.jp

In estrogen metabolism, the enzymatic properties of the 17ß-hydroxysteroid dehydrogenase (17ßHSD) isozymes play very important roles in steroid hormone metabolism in various tissues, including the placenta. 17ßHSD type 1 catalyzes primarily the reduction of estrone (E₁) to estradiol (E₂), whereas 17ßHSD type 2 catalyzes primarily the oxidation of E₂ to E₁. In this study, we examined immunohistochemical localization of 17ßHSD types 1 and 2 in human placenta (31 cases) ranging from 4–40 weeks gestation. The immunoreactivity of 17ßHSD type 1 was exclusively detected in syncytiotrophoblast from 4 weeks gestation to term placenta. Immunoreactivity of 17ßHSD type 2 first appeared in endothelial cells of intravillous vessels at 12 weeks gestation, and the number of 17ßHSD type 2-positive endothelial cells markedly increased up to 19 weeks, then reached a plateau. We quantitatively evaluated the 17ßHSD type 2-positive endothelial cells in chorionic villi and determined the ratio of 17ßHSD type 2-positive endothelial cells using immunohistochemistry of CD34, an endothelial antigen, in serial mirror tissue sections and subsequent image analysis using CAS 200. CD34 was detected from 4 weeks gestation, and its positive areas continued to increase toward term. The 17ßHSD type 2-positive area per CD34-positive area markedly increased from 13 weeks gestation and reached a plateau at 19 weeks gestation, in which almost all endothelial cells were positive for 17ßHSD type 2. 17ßHSD type 2, therefore, is considered to prevent the passage of excessive estrogens into the fetal circulation at endothelial cells of the intravillous fetal capillaries by catalyzing the inactivation of E₂ to E₁.

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