Skip Navigation


Mol. Hum. Reprod. Advance Access first published online on January 24, 2009
This version published online on February 10, 2009
Molecular Human Reproduction, doi:10.1093/molehr/gap005
This Article
Right arrow Advance Access manuscript (PDF) Freely available
Right arrow All Versions of this Article:
15/3/181    most recent
gap005v2
gap005v1
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 Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Bishop, C. V.
Right arrow Articles by Stouffer, R. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bishop, C. V.
Right arrow Articles by Stouffer, R. L.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2009. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

The effects of luteinizing hormone ablation/ replacement versus steroid ablation/ replacement on gene expression in the primate corpus luteum

Cecily V. Bishop1, Jon D. Hennebold1,2 and Richard L. Stouffer1,2

1Division of Reproductive Sciences, Oregon National Primate Research Center, Beaverton, OR, 97006 2Department of Obstetrics & Gynecology Oregon Health & Science University, Portland, OR, 97239

Corresponding Author: Dr Cecily Bishop bishopc{at}ohsu.edu 505 NW 185th Ave, Beaverton, OR, 97006 bishopc{at}ohsu.edu

This study was designed to provide a genome-wide analysis of the effects of LH versus steroid ablation/ replacement on gene expression in the developed corpus luteum (CL) in primates during the menstrual cycle. On days 9- 11 of the luteal phase, female rhesus monkeys were left untreated (Control) or received a GnRH antagonist Antide (A), A+LH, A+LH+ the 3β-HSD inhibitor Trilostane (TRL), or A+LH+TRL+ a progestin R5020. On Day 12 of the luteal phase, CL were removed and samples of RNA from individual CL were hybridized to AffymetrixTM rhesus macaque total genome microarrays. The greatest number of altered transcripts was associated with the ablation/ replacement of LH, while steroid ablation/ progestin replacement affected fewer transcripts. Replacement of LH during Antide treatment restored expression of most transcripts to control levels. Validation of a subset of transcripts revealed that expression patterns were similar between microarray and real-time PCR. Analyses of protein levels were subsequently determined for two transcripts. This is the first genome-wide analysis of LH and steroid regulation of gene transcription in the developed primate CL. Further analysis of novel transcripts identified in this data set can clarify the relative role for LH and steroids in CL maintenance and luteolysis.

Key Words: Corpus Luteum/Luteinizing Hormone/Microarray/Steroids/Progesterone

This study was funded by a grant from the National Institutes of Health (NIH), and is therefore subject to the NIH Public Access Policy (NOT-OD-08-033), in which the authors are obligated to submit their accepted manuscripts to the PubMed Central (PMC) archive (http://publicaccess.nih.gov/).

Submitted on October 13, 2008; resubmitted on January 13, 2009; accepted on January 21, 2009.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




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.