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Publication : Expression of mouse 17beta-hydroxysteroid dehydrogenase/17-ketosteroid reductase type 7 in the ovary, uterus, and placenta: localization from implantation to late pregnancy.

First Author  Nokelainen P Year  2000
Journal  Endocrinology Volume  141
Issue  2 Pages  772-8
PubMed ID  10650959 Mgi Jnum  J:60196
Mgi Id  MGI:1352961 Doi  10.1210/endo.141.2.7309
Citation  Nokelainen P, et al. (2000) Expression of mouse 17beta-hydroxysteroid dehydrogenase/17-ketosteroid reductase type 7 in the ovary, uterus, and placenta: localization from implantation to late pregnancy. Endocrinology 141(2):772-8
abstractText  Rodent 17beta-hydroxysteroid dehydrogenase/17-ketosteroid reductase type 7 (17HSD/KSR7) catalyzes the conversion of estrone (E1) to estradiol (E2) and is abundantly expressed in the ovaries of pregnant animals in particular. In the present work we demonstrate cell-specific expression of 17HSD/KSR7 in the ovaries, uteri, and placentas of pregnant and nonpregnant mice using in situ hybridization. The results show that mouse 17HSD/KSR7 (m17HSD/KSR7) messenger RNA is distinctly and exclusively expressed in a proportion of corpora lutea (CLs). During pregnancy, expression of m17HSD/KSR7 is most abundant around embryonic day 14.5 (E14.5), when the ovaries are filled with CLs expressing 17HSD/KSR7. In the uterus, m17HSD/KSR7 is first detected on E5.5, when expression surrounds the implantation site on the antimesometrial side. As gestation progresses, m17HSD/KSR7 is expressed in the decidua capsularis on E8 and E9.5, disappearing thereafter from the antimesometrial decidua. On E9 onward, m17HSD/KSR7 messenger RNA expression takes place at the junctional zone of the developing placenta. On E12.5 and E14.5, m17HSD/KSR7 is abundantly expressed in the spongiotrophoblasts, where expression gradually declines toward parturition. In conclusion, m17HSD/KSR7 expression in the CL is related to the life span of the CL. Moreover, spatial and temporal expression of m17HSD/KSR7 in the uterus suggests that locally produced E2 plays a role in implantation and/or decidualization. Finally, the results indicate that mouse placenta is capable of converting E1 to E2 in situ, and that the synthesized E2 may be effective in a paracrine, autocrine, and/or intracrine manner and be involved in placentation.
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