Presence and upregulation of Transient Receptor Potential Vanilloid 1 (TRPV1) and Ankyrin 1 (TRPA1) in translational rat endometriosis model

Krisztina Pohóczky, Noémi Bohonyi, M Elias Peter, Kajtár Béla, Helyes Zsuzsanna
In: Bulletin of Medical Sciences · 2019 · vol. 92(1) , pp. 15–26 · doi:10.2478/orvtudert-2019-0011 · W3006632616
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TRPV1 and TRPA1 mRNA were upregulated in chronic rat endometriosis lesions, and blocking capsaicin-sensitive nerve endings reduced lesion weight, validating this model for studying ion channel roles in endometriosis.

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The paper studied whether the non-selective cation channels TRPV1 and TRPA1 are present and upregulated in a translational rat model of peritoneal endometriosis, building on prior human data and earlier work showing estrogen-dependent expression in rat endometrium. Peritoneal endometriosis was surgically induced in 8-week-old female rats for either 2 weeks (acute) or 8 weeks (chronic), TRPA1/V1 mRNA levels were quantified by qPCR, and the role of capsaicin-sensitive sensory nerve endings was tested by ablating them with resiniferatoxin followed by lesion weight and size measurements. TRPV1 and TRPA1 mRNA were detected in normal rat endometrium, unchanged in sham animals, and in chronic—but not acute—endometriosis their expression was significantly elevated in lesions, paralleling human deep infiltrating endometriosis findings. Nerve ending elimination reduced lesion weight without affecting ectopic tissue size, and the authors frame the model as translationally suitable while noting its limitation to mRNA expression and functional inference. This paper is centrally about endometriosis — it uses a translational rat peritoneal endometriosis model to demonstrate chronic upregulation of TRPV1/TRPA1 and a sensory nerve–dependent effect on lesion weight.

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Abstract

Abstract The Transient Receptor Potential Vanilloid 1 (TRPV1) and Ankyrin 1 (TRPA1) are non-selective cation channels predominantly localized on capsaicin-sensitive sensory neurons; however both receptors have been described in non-neuronal tissues. It has been published that both receptors upregulated in peritoneal endometriosis in humans. Our research group demonstrated that TRPA1 and TRPV1 expression is elevated in human deep infiltrating endometriosis (DIE) lesions and the receptors have an estrogen-dependent expression pattern in rat endometrium. Here, we investigated the expression changes of TRPA1/V1 and the role of the capsaicin-sensitive sensory-nerve endings in a rat model of peritoneal endometriosis. Peritoneal endometriosis was surgically induced in 8-week-old female rats (n=7-7) for 2-weeks (acute condition) and 8-weeks (chronic condition). TRPA1/V1 mRNAs were quantified with quantitative polymerase chain reaction (qPCR). The expression levels were compared with the results obtained earlier from human DIE samples. The blockade of the TRPA1/V1 expressing capsaicin-sensitive nerve endings was induced with resiniferatoxin (RTX), followed by the measurement of the weight and size of the endometriosis lesions. We detected TRPV1 and TRPA1 mRNA in normal rat endometrium, their expression was not altered in sham-operated animals. In chronic, but not in acute endometriosis the expression was significantly elevated in the lesions, which results are consistent with our previous findings in human DIE. The elimination of capsaicin-sensitive nerve endings decreased the weight of the endometriosis lesions while the size of the ectopic tissue was not altered. Taken together, our results obtained from the rat endometriosis model are consistent with the previous human results, therefore this model is considered to have translational significance and it is suitable for functional analysis of the ion channels. The local, non-neuronal TRPA1 and TRPV1 might play a role in inflammation and sensory neuronal activation in endometriosis related pain, which is mediated by a broad range of pro-inflammatory molecules.
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Presence and upregulation of Transient Receptor Potential Vanilloid 1 (TRPV1) and Ankyrin 1 (TRPA1) in translational rat endometriosis model Abstract The Transient Receptor Potential Vanilloid 1 (TRPV1) and Ankyrin 1 (TRPA1) are non-selective cation channels predominantly localized on capsaicin-sensitive sensory neurons; however both receptors have been described in non-neuronal tissues. It has been published that both receptors upregulated in peritoneal endometriosis in humans. Our research group demonstrated that TRPA1 and TRPV1 expression is elevated in human deep infiltrating endometriosis (DIE) lesions and the receptors have an estrogen-dependent expression pattern in rat endometrium. Here, we investigated the expression changes of TRPA1/V1 and the role of the capsaicin-sensitive sensory-nerve endings in a rat model of peritoneal endometriosis. Peritoneal endometriosis was surgically induced in 8-week-old female rats (n=7-7) for 2-weeks (acute condition) and 8-weeks (chronic condition). TRPA1/V1 mRNAs were quantified with quantitative polymerase chain reaction (qPCR). The expression levels were compared with the results obtained earlier from human DIE samples. The blockade of the TRPA1/V1 expressing capsaicin-sensitive nerve endings was induced with resiniferatoxin (RTX), followed by the measurement of the weight and size of the endometriosis lesions. We detected TRPV1 and TRPA1 mRNA in normal rat endometrium, their expression was not altered in sham-operated animals. In chronic, but not in acute endometriosis the expression was significantly elevated in the lesions, which results are consistent with our previous findings in human DIE. The elimination of capsaicin-sensitive nerve endings decreased the weight of the endometriosis lesions while the size of the ectopic tissue was not altered. Taken together, our results obtained from the rat endometriosis model are consistent with the previous human results, therefore this model is considered to have translational significance and it is suitable for functional analysis of the ion channels. The local, non-neuronal TRPA1 and TRPV1 might play a role in inflammation and sensory neuronal activation in endometriosis related pain, which is mediated by a broad range of pro-inflammatory molecules. © 2020 Pohóczky Krisztina, Bohonyi Noémi, Maczkó Péter, Kajtár Béla, Helyes Zsuzsanna, published by Transylvanian Museum Society This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

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