Skip Navigation



Hum. Reprod. Advance Access published online on May 28, 2009

Human Reproduction, doi:10.1093/humrep/dep192
This Article
Right arrow Full Text
Right arrow Full Text (PDF )
Right arrow All Versions of this Article:
24/9/2193    most recent
dep192v1
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
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 Bellehumeur, C.
Right arrow Articles by Akoum, A.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bellehumeur, C.
Right arrow Articles by Akoum, A.
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

Interleukin 1 regulates its own receptors in human endometrial cells via distinct mechanisms

C. Bellehumeur1, J. Blanchet2, J.-Y. Fontaine2, N. Bourcier1 and A. Akoum1,2,3

1 Unité d'Endocrinologie de la Reproduction, Centre de Recherche, Hôpital Saint-François d'Assise, Centre Hospitalier Universitaire de Québec, 10 rue de l'Espinay, Local D0-711, Québec, Québec, Canada G1L 3L5 2 Département d'Obstétrique et Gynécologie, Faculté de Médecine, Université Laval, Québec, Canada

3 Correspondence address. Tel: +1-418-525-4444/53329; Fax: +1-418-525-4195; E-mail: ali.akoum{at}crsfa.ulaval.ca

BACKGROUND: Interleukin 1 (IL1) plays an important role in the physiology of human endometrium and is recognized as a major and early embryonic signal. Tight control over the local endometrial action of this cytokine is critical for normal reproductive functions. The coordinated regulation of IL1 receptors types I and II (IL1R1 and IL1R2) and IL1 receptor antagonist (IL1RA) in endometrial cells may represent one of the principle mechanisms involved in the control of IL1 local effects. The objective of this study was to investigate the regulation of IL1Rs in human endometrial epithelial cells in response to IL1.

METHODS: Cultures of KLE endometrial epithelial cell line and primary human endometrial epithelial cells, immunofluorescent staining, enzyme-linked immunosorbent assay, western blotting, nuclear transcription (run-on) and real-time PCR were used to investigate the expression of IL1R1, IL1R2 and IL1RA.

RESULTS: Cells appeared to react to IL1 by up-regulating the expression of the signaling activating IL1R1 and to moderate in parallel IL1 effects by elevating the expression of the decoy inhibitory IL1R2 and the receptor antagonist IL1RA. Regulation of IL1R1 and IL1RA by IL1B involved gene transcription activation and that of IL1R2 involved mRNA stabilization.

CONCLUSION: Considering IL1's immunomodulatory, proangiogenic and tissue remodeling properties, and its role as an embryonic signal, modulation of endometrial cell responsiveness to IL1 via the concomitant regulation of its own activating and inhibitory receptors and receptor antagonist may represent an important regulatory mechanism of IL1-induced physiological changes occurring in the human endometrium during the normal menstrual cycle and embryo development.

Key words: human endometrium/IL1/receptors

Submitted on August 20, 2008; resubmitted on April 7, 2009; accepted on April 22, 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.