Results
| PMID | 23553861 |
| Gene Name | TACR2 |
| Condition | Endometriosis |
| Association |
Associated |
| Mutation | FCRL3 -169T>C |
| Sex | Female |
| Associated genes | TACR1, TACR2 |
| Other associated phenotypes |
Endometriosis |
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J Clin Endocrinol Metab. 2013 Jun;98(6):2469-77. doi: 10.1210/jc.2013-1019. Epub McKinnon, Brett D| Evers, Jakob| Bersinger, Nick A| Mueller, Michael D Department of Obstetrics and Gynaecology, Inselspital, University of Berne, Berne, CH-3010, Switzerland. brett.mckinnon@dkf.unibe.ch CONTEXT: Endometriosis is characterized by the growth of ectopic endometrial tissue. Nerve fibers are frequently associated with ectopic lesions, and neurogenic inflammation may play a role in endometriosis. OBJECTIVE: The purpose of this study was to determine the presence of tachykinin receptors in endometriotic lesions and the role of TNFalpha on their expression. DESIGN: This study was an assessment of matching eutopic and ectopic endometrial tissue and peritoneal fluid from patients with endometriosis and an in vitro analysis of primary endometrial cells. SETTING: The setting was a university hospital. PATIENTS: Participants were premenopausal women undergoing laparoscopy. INTERVENTIONS: Endometriotic lesions were removed surgically. MAIN OUTCOME MEASURES: Tachykinin mRNA (TACR1/2) and protein (neurokinin 1 receptor [NK1R]) expression in both eutopic and ectopic endometrial tissue from patients with endometriosis and the correlation to peritoneal fluid TNFalpha were measured. Primary endometrial epithelial and stromal cells were assessed in vitro to determine the induction of TACR1/2 and NK1R expression after TNFalpha treatment. Cell viability of endometrial stromal cells after substance P exposure was also assessed. RESULTS: Expression of both TACR1 and TACR2 mRNA was significantly higher in the ectopic than in the eutopic tissue. Both TACR1 mRNA and NK1R protein expression was significantly correlated with peritoneal fluid TNFalpha, and in vitro studies confirmed that TNFalpha treatment induced both TACR1 mRNA and NK1R protein expression in endometrial stromal cells. In endometrial stromal cells, substance P treatment enhanced cell viability, which was inhibited by a specific NK1R antagonist. CONCLUSIONS: NK1R expression is induced in ectopic endometrial tissue by peritoneal TNFalpha. Induction of NK1R expression may permit endometriotic lesion maintenance via exposure to substance P. Mesh Terms: Endometriosis/*etiology/pathology| Endometrium/drug effects/metabolism| Female| Humans| Neurokinin-1 Receptor Antagonists| RNA, Messenger/analysis| Receptors, Neurokinin-1/analysis/*physiology| Receptors, Tachykinin/genetics| Substance P/pharmacol |
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