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17ß-Hydroxysteroid Dehydrogenase Type 1 and 2 Expression in the Human Fetus¹

Department of Pathology (J.T., T.S., G.H., Y.M., H.N., H.S.) and Pediatrics (J.T., K.I.), Tohoku University School of Medicine, Sendai, Miyagi 980-8575; Research Institute of Life Science, Snow Brand Co. Ltd. (J.N., K.K., M.Y.), Tochigi 329-0512; and the Division of Molecular Genetics, Institute for Comprehensive Medical Science, Fujita Health University (N.H.), Toyoake, Aichi 470-1192, Japan; and the 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: Dr. Junji Takeyama, Department of Pathology, Tohoku University School of Medicine, 2–1 Seiryo-machi, Aoba-ku, Sendai, Miyagi 980-8575, Japan. E-mail: j-takeyama{at}patholo2.med.tohoku.ac.jp

The present study investigates the expression patterns of 17ß-hydroxysteroid dehydrogenase (17ßHSD) isozymes in human fetal tissues to understand how estrogenic activity is regulated in the human fetus. Using enzyme assay, high 17ßHSD activity was detected in the placenta and liver, and low levels of 17ßHSD activity were also present in the gastrointestinal tract and kidney. After Northern blot analysis, we detected the messenger ribonucleic acid for 17ßHSD type 1 (17ßHSD1) only in the placenta, whereas that for 17ßHSD type 2 (17ßHSD2) was detected in the placenta, liver, gastrointestinal tract, and urinary tract at 20 gestational weeks. In RT-PCR analysis of the messenger ribonucleic acid transcripts, 17ßHSD1 was predominantly expressed in the placenta, brain, heart, lung, and adrenal, whereas 17ßHSD2 expression was predominantly detected in the liver, gastrointestinal tract, and kidney. In addition, we detected 17ßHSD2 immunoreactive protein in surface epithelial cells of the stomach, absorptive epithelial cells of the small intestine and colon, hepatocytes of the liver, and interstitial cells surrounding the urinary tubules of the renal medulla. 17ßHSD2 in these tissues may be functioning in the prevention of in utero exposure of the fetus to excessive estradiol from the maternal circulation and amniotic fluids.

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