Skip Navigation

This Article
Right arrow FREE Full Text (PDF) Freely available
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 ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (8)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Chen, Z. G.
Right arrow Articles by Dong, K. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Chen, Z. G.
Right arrow Articles by Dong, K. W.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Molecular Human Reproduction, Vol 4, 93-99, Copyright © 1998 by Oxford University Press

JOURNAL ARTICLE

Glucocorticoids modulate human gonadotrophin releasing hormone upstream promoter activity in transfected human placental cells (JEG-3)

ZG Chen, CS Chou, MI Hsu and KW Dong
Jones Institute for Reproductive Medicine, Eastern Virginia Medical School, Norfolk 23507, USA.

A human gonadotrophin releasing hormone (GnRH) upstream promoter/luciferase reporter gene construct (H2 construct) was generated by inserting a 1.7 kb XbaI/AflII fragment containing the human GnRH upstream promoter region only into a promoter-less luciferase reporter vector. When JEG-3 cells were transiently transfected with this construct and treated with cortisol or its synthetic analogue dexamethasone, a stimulatory effect on the upstream promoter activity was observed. This stimulation was dependent on the cotransfection of a glucocorticoid receptor (GR) cDNA expression vector due to the low level of GR in JEG-3 cells and could be completely abolished by RU486, a glucocorticoid antagonist. Moreover, the cortisol actions could be modulated to a different extent by oestradiol. Thus, since the human placenta contains GRs and the increase in cortisol metabolism near term is regulated by oestrogen, the current findings suggest that cortisol may be physiologically involved in the regulation of GnRH gene expression in the human placenta.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Mol Hum ReprodHome page
T.A. Bramley, K. Campbell, and G.S. Menzies
Human placental GnRH-like factors: II. Inhibition of enzymatic degradation of GnRH-II and [D-Trp6]GnRH ethylamide tracers by human term placental cytosol fractions reveals the presence of GnRH-binding protein(s)
Mol. Hum. Reprod., May 1, 2003; 9(5): 291 - 300.
[Abstract] [Full Text] [PDF]

Home page
 Mol Hum ReprodHome page
S. Santra, V. S. Rao, Y.G. Shanker, and A.J. Rao
Cloning and characterization of bonnet monkey GnRH receptor
Mol. Hum. Reprod., May 1, 2000; 6(5): 415 - 421.
[Abstract] [Full Text] [PDF]

Home page
 Mol Hum ReprodHome page
T.A. Bramley and G.S. Menzies
Human placental gonadotrophin-releasing hormone-like factors: an artefact of human placental peptidases?
Mol. Hum. Reprod., February 1, 2000; 6(2): 113 - 126.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.