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Hum. Reprod. Advance Access published online on September 25, 2006
Human Reproduction, doi:10.1093/humrep/del368
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© The Author 2006. 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
Received April 4, 2006
Revised July 17, 2006
Accepted August 9, 2006

Article

Both GnRH agonist and continuous oral progestin treatments reduce the expression of the tyrosine kinase receptor B and mu-opioid receptor in deep infiltrating endometriosis

S. Matsuzaki 1 *, M. Canis 1, J.-L. Pouly 1, R. Botchorishvili 1, P.J. Déchelotte 2, and G. Mage 1

1 CHU Clermont-Ferrand, Polyclinique-Hôtel-Dieu, Gynécologie Obstétrique et Médecine de la Reproduction, Clermont-Ferrand, France
2 Anatomie et cytologie pathologiques, Clermont-Ferrand, France

* To whom correspondence should be addressed.
S. Matsuzaki, E-mail: sachikoma{at}aol.com


  Abstract

BACKGROUND: Deep infiltrating endometriosis (DIE) is commonly associated with severe pain. The pain can be managed successfully with GnRH agonists or continuous progestins. The precise molecular mechanism by which DIE causes pain or why hormonal treatment is effective, however, remains unclear. We recently identified three potential candidate genes that might be involved in DIE pain pathways: tyrosine kinase receptor B (TrKB), mu-opioid receptor (MOR) and serotonin transporter (5HTT). We hypothesized that if these three genes were involved in DIE-associated pain, their expression levels would probably be modulated by GnRH agonist or progestin. In this study, we compared mRNA expression levels of TrKB, MOR and 5HTT in DIE among patients pre-operatively treated with GnRH agonist, progestin or without pre-operative medical treatments. METHODS: The expression levels of TrKB, MOR and 5HTT mRNA in DIE were determined using laser capture microdissection and real-time RT-PCR techniques. RESULTS: The expression levels of TrKB in epithelial cells and MOR in stromal cells from DIE were significantly decreased in patients with pre-operative GnRH agonist or progestin. There was no significant difference in 5HTT expression levels among untreated, GnRH agonist- and progestin-treated patients. CONCLUSION: The expression levels of TrKB and MOR genes in DIE appeared to be modulated by GnRH agonist or progestin. However, the functional roles of TrKB and MOR in DIE remain to be clarified.

Keywords: deep infiltrating endometriosis/endometriosis-associated pain/laser capture microdissection.

Presented in part at the 61st Annual Meeting of the American Society for Reproductive Medicine, Montréal, Quebéc, Canada (October 15-19, 2005).


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