Biol Reprod Keystone Symposia Conference on Frontiers in Reproductive Biology & Regulation of Fertility.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 QUICK SEARCH:   [advanced]


     


BOR - Papers in Press, published online ahead of print May 30, 2007.
Biol Reprod 2007, 10.1095/biolreprod.106.059451
This Article
Right arrow Full Text (Rapid PDF)
Right arrow All Versions of this Article:
77/3/517    most recent
biolreprod.106.059451v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Su, E. J.
Right arrow Articles by Bulun, S. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Su, E. J.
Right arrow Articles by Bulun, S. E.
Agricola
Right arrow Articles by Su, E. J.
Right arrow Articles by Bulun, S. E.
Submitted January 3, 2007
Returned for revision January 11, 2007
Accepted May 24, 2007

Pregnancy


Regulation of 17-beta Hydroxysteroid Dehydrogenase Type 2 in Human Placental Endothelial Cells

Emily J. Su , You-Hong Cheng , Robert T. Chatterton , Zhi-Hong Lin , Ping Yin , Scott Reierstad , Joy Innes , and Serdar E. Bulun *

* To whom correspondence should be addressed. E-mail: s-bulun{at}northwestern.edu.

Abstract
17-beta hydroxysteroid dehydrogenase type 2 (HSD17B2) oxidizes estradiol to estrone, testosterone to androstenedione, and 20 alpha-dihydroprogesterone to progesterone. HSD17B2 is highly expressed in human placental tissue where it is localized to placental endothelial cells lining the fetal compartment. The aim of this study was to investigate the effects of potential regulatory factors including progesterone, estradiol, and retinoic acid (RA) on HSD17B2 expression in primary human placental endothelial cells in culture. HSD17B2 mRNA expression was not regulated by progesterone, the progesterone agonist R5020, or estradiol treatment. RA significantly induced HSD17B2 mRNA levels and enzyme activity in a dose- and time-dependent manner. Maximal stimulation occurred at 48-hours at a RA concentration of 10-6 M. Both retinoic acid receptor alpha (RARA) and retinoid x receptor alpha (RXRA) were readily detected by immunoblotting in isolated placental endothelial cells. RNA interference (RNAi) directed against RARA or RXRA led to reduced basal levels of HSD17B2 mRNA levels and significantly abolished RA-stimulated HSD17B2 expression. Together, these data indicate that regulation of HSD17B2 mRNA levels and enzymatic activity by RA in the placenta is mediated by RARA and RXRA.

Key words: Pregnancy • Placenta • Steroid hormones • Steroid hormone receptors


This article has been cited by other articles:


Home page
J. Clin. Endocrinol. Metab.Home page
Y.-H. Cheng, P. Yin, Q. Xue, B. Yilmaz, M. I. Dawson, and S. E. Bulun
Retinoic Acid (RA) Regulates 17{beta}-Hydroxysteroid Dehydrogenase Type 2 Expression in Endometrium: Interaction of RA Receptors with Specificity Protein (SP) 1/SP3 for Estradiol Metabolism
J. Clin. Endocrinol. Metab., May 1, 2008; 93(5): 1915 - 1923.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Copyright © 2007 by the Society for the Study of Reproduction.