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.
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.


CONCLUSIONS
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.
Matsuzaki
S
S
CHU Clermont-Ferrand, Polyclinique-Hôtel-Dieu, Gynécologie Obstétrique et Médecine de la Reproduction, France. sachikoma@aol.com
Canis
M
M
Pouly
J-L
JL
Botchorishvili
R
R
Déchelotte
P J
PJ
Mage
G
G
D000328:Adult; D004715:Endometriosis / Q000188:drug therapy* / Q000378:metabolism*; D004717:Endometrium / Q000378:metabolism*; D005260:Female; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation / Q000187:drug effects*; D007987:Gonadotropin-Releasing Hormone / Q000819:agonists*; D006801:Humans; D017699:Pelvic Pain / Q000378:metabolism; D011374:Progesterone / Q000627:therapeutic use*; D020813:Receptor, trkB / Q000096:biosynthesis*; D017450:Receptors, Opioid, mu / Q000096:biosynthesis*
D017450:Receptors, Opioid, mu; D007987:Gonadotropin-Releasing Hormone; D011374:Progesterone; D020813:Receptor, trkB