Human 17β-Hydroxysteroid Dehydrogenase Type 2 Messenger Ribonucleic Acid Expression and Localization in Term Placenta and in Endometrium during the Menstrual Cycle1
Author(s) -
Mika Mustonen,
Veli Isomaa,
Tommi Vaskivuo,
Juha S. Tapanainen,
Matti Poutanen,
Frej Stenbäck,
Reijo Vihko,
Pirkko Vihko
Publication year - 1998
Publication title -
the journal of clinical endocrinology and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.206
H-Index - 353
eISSN - 1945-7197
pISSN - 0021-972X
DOI - 10.1210/jcem.83.4.4709
Subject(s) - endometrium , endocrinology , medicine , luteal phase , hydroxysteroid dehydrogenase , estrone , placenta , syncytiotrophoblasts , biology , estrogen , menstrual cycle , messenger rna , gene expression , in situ hybridization , dehydrogenase , chemistry , follicular phase , enzyme , hormone , biochemistry , gene , fetus , pregnancy , genetics
According to the current hypothesis, 17beta-hydroxysteroid dehydrogenases (17HSDs) regulate the extent of estrogen influence in the endometrium by converting estradiol (E2) locally into a biologically less active sex steroid, estrone (E1), and vice versa. Recently, we have shown that both 17HSD type 1 and type 2 are expressed in the human endometrium, and in the present work, using in situ hybridization, we show that 17HSD type 2 is localized in the glandular epithelial cells as previously shown for the type 1 enzyme, but in contrast to type 1, the expression of type 2 is highest at the end of the cycle. Hence, we hypothesize that the differential expression of the two 17HSD enzymes, with opposite activities in same cell types, could modulate intracellular E2 concentrations during the end of the luteal phase of the menstrual cycle. We further analyzed the expression of 17HSD type 1 and type 2 mRNAs in term human placenta. Expression of 17HSD type 1 mRNA was detected in the syncytiotrophoblasts, and signals for type 2 mRNA were found inside the villi, corresponding to cytotrophoblasts. The expression of 17HSD type 2 in the placenta may serve to maintain the presence of inactive sex steroids and attenuate the formation of biologically potent androgens and estrogens.
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