Induction of the Neurokinin 1 Receptor by TNFα in Endometriotic Tissue Provides the Potential for Neurogenic Control Over Endometriotic Lesion Growth
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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 TNFα 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 TNFα were measured. Primary endometrial epithelial and stromal cells were assessed in vitro to determine the induction of TACR1/2 and NK1R expression after TNFα 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 TNFα, and in vitro studies confirmed that TNFα 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 TNFα. Induction of NK1R expression may permit endometriotic lesion maintenance via exposure to substance P.
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Expression of NK1R and SP-coding gene TAC1 is upregulated by estrogen and TNF-α.
“The expression of NK1R and SP-coding gene TAC1 is reported to be upregulated by estrogen68,71 and TNF-α44.”
From Neuropeptides Substance P and Calcitonin Gene Related Peptide Accelerate the Development and Fibrogenesis of Endometriosis (2019) · cites this paper as [44]
The endogenous receptor for substance P is neurokinin 1 receptor (NK1R).
“The endogenous receptor for SP is NK1R44”
From Neuropeptides Substance P and Calcitonin Gene Related Peptide Accelerate the Development and Fibrogenesis of Endometriosis (2019) · cites this paper as [44]
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References 46 · Cited by 32
Research works printed but not linked: 4
- Lebovic DI, Mueller MD, Taylor RN. Immunobiology of endome- triosis. Fertil Steril. 2001;75:1-10.
- McGillis JP, Mitsuhashi M, Payan DG. Immunomodulation by tachykinin neuropeptides. Ann NY Acad Sci. 1990;594:85-94.
- Mantyh CR, Maggio JE, Mantyh PW, Vigna SR, Pappas TN. In- creased substance P receptor expression by blood vessels and lym- phoid aggregates in Clostridium difficile-induced pseudomembra- nous colitis. Dig Dis Sci. 1996;41:614 -620.
- Karck U, Reister F, Schäfer W, Zahradnik HP, Breckwoldt M. PGE 2 and PGF 2␣ release by human peritoneal macrophages in endome- triosis. Prostaglandins. 1996;51:49 -60.
- Authors
- McKinnon, B. D., Evers, J., Bersinger, N. A., & Mueller, M. D.
- Affiliations
- University of Bern (CH)
- Corresponding author
- McKinnon, Brett D.
- Venue
- The Journal of Clinical Endocrinology & Metabolism
- Publisher
- The Endocrine Society
- Published
- 2013-06-01
- Volume
- 98
- Issue
- 6
- Pages
- 2469-2477
- ISSN
- 0021-972X (ISSN-L)
- 1945-7197
- OpenAlex
- W1986186718
- Cited by
- 32
- References
- 46
- Citations by year
- 2026: 3 · 2024: 6 · 2023: 2 · 2022: 1 · 2021: 6 · 2020: 2 · 2019: 1 · 2018: 1 · 2017: 3 · 2016: 4 · 2015: 2 · 2014: 1
- FWCI
- 2.81
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
- PubMed (publishedVersion)
- BORIS (University Library Bern) (submittedVersion, other-oa)
- Open Access CRIS of the University of Bern
- Topics
- Health Sciences › Medicine › Reproductive Medicine › Endometriosis Research and Treatment
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Life Sciences › Agricultural and Biological Sciences › Ecology, Evolution, Behavior and Systematics › Plant and fungal interactions
- Keywords
- endometriosis, neurokinin-1 receptor, TNF-α, tachykinin receptors, substance P, neurogenic inflammation, endometriotic lesions, endometrial stromal cells, peritoneal fluid, ectopic endometrium
- MeSH terms
- Endometriosis, Endometrium, Female, Humans, RNA, Messenger, Substance P, Tumor Necrosis Factor-alpha, Receptors, Tachykinin, Receptors, Neurokinin-1, Neurokinin-1 Receptor Antagonists
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