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Academic literature on the topic 'TRPA1'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 March 2023

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Journal articles on the topic "TRPA1"

1

Bousquet, Jean, Wienczyslawa Czarlewski, Torsten Zuberbier, Joaquim Mullol, Hubert Blain, Jean-Paul Cristol, Rafael De La Torre, et al. "Potential Interplay between Nrf2, TRPA1, and TRPV1 in Nutrients for the Control of COVID-19." International Archives of Allergy and Immunology 182, no. 4 (2021): 324–38. http://dx.doi.org/10.1159/000514204.

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In this article, we propose that differences in COVID-19 morbidity may be associated with transient receptor potential ankyrin 1 (TRPA1) and/or transient receptor potential vanilloid 1 (TRPV1) activation as well as desensitization. TRPA1 and TRPV1 induce inflammation and play a key role in the physiology of almost all organs. They may augment sensory or vagal nerve discharges to evoke pain and several symptoms of COVID-19, including cough, nasal obstruction, vomiting, diarrhea, and, at least partly, sudden and severe loss of smell and taste. TRPA1 can be activated by reactive oxygen species and may therefore be up-regulated in COVID-19. TRPA1 and TRPV1 channels can be activated by pungent compounds including many nuclear factor (erythroid-derived 2) (Nrf2)-interacting foods leading to channel desensitization. Interactions between Nrf2-associated nutrients and TRPA1/TRPV1 may be partly responsible for the severity of some of the COVID-19 symptoms. The regulation by Nrf2 of TRPA1/TRPV1 is still unclear, but suggested from very limited clinical evidence. In COVID-19, it is proposed that rapid desensitization of TRAP1/TRPV1 by some ingredients in foods could reduce symptom severity and provide new therapeutic strategies.
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Zhang, Hongyu, Peter J. Wickley, Sayantani Sinha, Ian N. Bratz, and Derek S. Damron. "Propofol Restores Transient Receptor Potential Vanilloid Receptor Subtype-1 Sensitivity via Activation of Transient Receptor Potential Ankyrin Receptor Subtype-1 in Sensory Neurons." Anesthesiology 114, no. 5 (May 1, 2011): 1169–79. http://dx.doi.org/10.1097/aln.0b013e31820dee67.

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Background Cross talk between peripheral nociceptors belonging to the transient receptor potential vanilloid receptor subtype-1 (TRPV1) and ankyrin subtype-1 (TRPA1) family has been demonstrated recently. Moreover, the intravenous anesthetic propofol has directly activates TRPA1 receptors and indirectly restores sensitivity of TRPV1 receptors in dorsal root ganglion (DRG) sensory neurons. Our objective was to determine the extent to which TRPA1 activation is involved in mediating the propofol-induced restoration of TRPV1 sensitivity. Methods Mouse DRG neurons were isolated by enzymatic dissociation and grown for 24 h. F-11 cells were transfected with complementary DNA for both TRPV1 and TRPA1 or TRPV1 only. The intracellular Ca concentration was measured in individual cells via fluorescence microscopy. After TRPV1 desensitization with capsaicin (100 nM), cells were treated with propofol (1, 5, and 10 μM) alone or with propofol in the presence of the TRPA1 antagonist, HC-030031 (0.5 μM), or the TRPA1 agonist, allyl isothiocyanate (AITC; 100 μM); capsaicin was then reapplied. Results In DRG neurons that contain both TRPV1 and TRPA1, propofol and AITC restored TRPV1 sensitivity. However, in DRG neurons containing only TRPV1 receptors, exposure to propofol or AITC after desensitization did not restore capsaicin-induced TRPV1 sensitivity. Similarly, in F-11 cells transfected with both TRPV1 and TRPA1, propofol and AITC restored TRPV1 sensitivity. However, in F-11 cells transfected with TRPV1 only, neither propofol nor AITC was capable of restoring TRPV1 sensitivity. Conclusions These data demonstrate that propofol restores TRPV1 sensitivity in primary DRG neurons and in cultured F-11 cells transfected with both the TRPV1 and TRPA1 receptors via a TRPA1-dependent process. Propofol's effects on sensory neurons may be clinically important and may contribute to peripheral sensitization to nociceptive stimuli in traumatized tissue.
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Kiss, Fruzsina, Viktória Kormos, Éva Szőke, Angéla Kecskés, Norbert Tóth, Anita Steib, Árpád Szállási, et al. "Functional Transient Receptor Potential Ankyrin 1 and Vanilloid 1 Ion Channels Are Overexpressed in Human Oral Squamous Cell Carcinoma." International Journal of Molecular Sciences 23, no. 3 (February 8, 2022): 1921. http://dx.doi.org/10.3390/ijms23031921.

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Oral squamous cell carcinoma (OSCC) is a common cancer with poor prognosis. Transient Receptor Potential Ankyrin 1 (TRPA1) and Vanilloid 1 (TRPV1) receptors are non-selective cation channels expressed on primary sensory neurons and epithelial and immune cells. TRPV1 mRNA and immunopositivity, as well as TRPA1-like immunoreactivity upregulation, were demonstrated in OSCC, but selectivity problems with the antibodies still raise questions and their functional relevance is unclear. Therefore, here, we investigated TRPA1 and TRPV1 expressions in OSCC and analyzed their functions. TRPA1 and TRPV1 mRNA were determined by RNAscope in situ hybridization and qPCR. Radioactive 45Ca2+ uptake and ATP-based luminescence indicating cell viability were measured in PE/CA-PJ41 cells in response to the TRPA1 agonist allyl-isothiocyanate (AITC) and TRPV1 agonist capsaicin to determine receptor function. Both TRPA1 and TRPV1 mRNA are expressed in the squamous epithelium of the human oral mucosa and in PE/CA-PJ41 cells, and their expressions are significantly upregulated in OSCC compared to healthy mucosa. TRPA1 and TRPV1 activation (100 µM AITC, 100 nM capsaicin) induced 45Ca2+-influx into PE/CA-PJ41 cells. Both AITC (10 nM–5 µM) and capsaicin (100 nM–45 µM) reduced cell viability, reaching significant decrease at 100 nM AITC and 45 µM capsaicin. We provide the first evidence for the presence of non-neuronal TRPA1 receptor in the OSCC and confirm the expression of TRPV1 channel. These channels are functionally active and might regulate cancer cell viability.
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Zhao, Huan, Leslie K. Sprunger, and Steven M. Simasko. "Expression of transient receptor potential channels and two-pore potassium channels in subtypes of vagal afferent neurons in rat." American Journal of Physiology-Gastrointestinal and Liver Physiology 298, no. 2 (February 2010): G212—G221. http://dx.doi.org/10.1152/ajpgi.00396.2009.

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Vagal afferent neurons relay important information regarding the control of the gastrointestinal system. However, the ionic mechanisms that underlie vagal activation induced by sensory inputs are not completely understood. We postulate that transient receptor potential (TRP) channels and/or two-pore potassium (K2p) channels are targets for activating vagal afferents. In this study we explored the distribution of these channels in vagal afferents by quantitative PCR after a capsaicin treatment to eliminate capsaicin-sensitive neurons, and by single-cell PCR measurements in vagal afferent neurons cultured after retrograde labeling from the stomach or duodenum. We found that TRPC1/3/5/6, TRPV1-4, TRPM8, TRPA1, TWIK2, TRAAK, TREK1, and TASK1/2 were all present in rat nodose ganglia. Both lesion results and single-cell PCR results suggested that TRPA1 and TRPC1 were preferentially expressed in neurons that were either capsaicin sensitive or TRPV1 positive. Expression of TRPM8 varied dynamically after various manipulations, which perhaps explains the disparate results obtained by different investigators. Last, we also examined ion channel distribution with the A-type CCK receptor (CCK-RA) and found there was a significant preference for neurons that express TRAAK to also express CCK-RA, especially in gut-innervating neurons. These findings, combined with findings from prior studies, demonstrated that background conductances such as TRPC1, TRPA1, and TRAAK are indeed differentially distributed in the nodose ganglia, and not only do they segregate with specific markers, but the degree of overlap is also dependent on the innervation target.
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Payrits, Maja, Ádám Horváth, Tünde Biró-Sütő, János Erostyák, Géza Makkai, Éva Sághy, Krisztina Pohóczky, et al. "Resolvin D1 and D2 Inhibit Transient Receptor Potential Vanilloid 1 and Ankyrin 1 Ion Channel Activation on Sensory Neurons via Lipid Raft Modification." International Journal of Molecular Sciences 21, no. 14 (July 16, 2020): 5019. http://dx.doi.org/10.3390/ijms21145019.

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Transient Receptor Potential Vanilloid 1 and Ankyrin 1 (TRPV1, TRPA1) cation channels are expressed in nociceptive primary sensory neurons and regulate nociceptor and inflammatory functions. Resolvins are endogenous lipid mediators. Resolvin D1 (RvD1) is described as a selective inhibitor of TRPA1-related postoperative and inflammatory pain in mice acting on the G protein-coupled receptor DRV1/GPR32. Resolvin D2 (RvD2) is a very potent TRPV1 and TRPA1 inhibitor in DRG neurons, and decreases inflammatory pain in mice acting on the GPR18 receptor, via TRPV1/TRPA1-independent mechanisms. We provided evidence that resolvins inhibited neuropeptide release from the stimulated sensory nerve terminals by TRPV1 and TRPA1 activators capsaicin (CAPS) and allyl-isothiocyanate (AITC), respectively. We showed that RvD1 and RvD2 in nanomolar concentrations significantly decreased TRPV1 and TRPA1 activation on sensory neurons by fluorescent calcium imaging and inhibited the CAPS- and AITC-evoked 45Ca-uptake on TRPV1- and TRPA1-expressing CHO cells. Since CHO cells are unlikely to express resolvin receptors, resolvins are suggested to inhibit channel opening through surrounding lipid raft disruption. Here, we proved the ability of resolvins to alter the membrane polarity related to cholesterol composition by fluorescence spectroscopy. It is concluded that targeting lipid raft integrity can open novel peripheral analgesic opportunities by decreasing the activation of nociceptors.
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Wilzopolski, Jenny, Manfred Kietzmann, Santosh K. Mishra, Holger Stark, Wolfgang Bäumer, and Kristine Rossbach. "TRPV1 and TRPA1 Channels Are Both Involved Downstream of Histamine-Induced Itch." Biomolecules 11, no. 8 (August 6, 2021): 1166. http://dx.doi.org/10.3390/biom11081166.

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Two histamine receptor subtypes (HR), namely H1R and H4R, are involved in the transmission of histamine-induced itch as key components. Although exact downstream signaling mechanisms are still elusive, transient receptor potential (TRP) ion channels play important roles in the sensation of histaminergic and non-histaminergic itch. The aim of this study was to investigate the involvement of TRPV1 and TRPA1 channels in the transmission of histaminergic itch. The potential of TRPV1 and TRPA1 inhibitors to modulate H1R- and H4R-induced signal transmission was tested in a scratching assay in mice in vivo as well as via Ca2+ imaging of murine sensory dorsal root ganglia (DRG) neurons in vitro. TRPV1 inhibition led to a reduction of H1R- and H4R- induced itch, whereas TRPA1 inhibition reduced H4R- but not H1R-induced itch. TRPV1 and TRPA1 inhibition resulted in a reduced Ca2+ influx into sensory neurons in vitro. In conclusion, these results indicate that both channels, TRPV1 and TRPA1, are involved in the transmission of histamine-induced pruritus.
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Kunkler, Phillip Edward, LuJuan Zhang, Jessica Joan Pellman, Gerry Stephen Oxford, and Joyce Harts Hurley. "Sensitization of the trigeminovascular system following environmental irritant exposure." Cephalalgia 35, no. 13 (February 27, 2015): 1192–201. http://dx.doi.org/10.1177/0333102415574845.

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Background Air pollution is linked to increased emergency room visits for headache, and migraine patients frequently cite chemicals or odors as headache triggers, but the association between air pollutants and headache is not well understood. We previously reported that nasal administration of environmental irritants acutely increases meningeal blood flow via a TRPA1-dependent mechanism involving the trigeminovascular system. Here, we examine whether chronic environmental irritant exposure sensitizes the trigeminovascular system. Methods Male rats were exposed to acrolein, a TRPA1 agonist, or room air by inhalation for four days prior to meningeal blood flow measurements. Some animals were injected daily with a TRPA1 antagonist, AP-18, or vehicle prior to inhalation exposure. Trigeminal ganglia were isolated following blood flow measurements for immunocytochemistry and/or qPCR determination of TRPV1, TRPA1 and CGRP levels. Results Acrolein inhalation exposure potentiated blood flow responses both to TRPA1 and TRPV1 agonists compared to room air. Acrolein exposure did not alter TRPV1 or TRPA1 mRNA levels or TRPV1 or CGRP immunoreactive cell counts in the trigeminal ganglion. Acrolein sensitization of trigeminovascular responses to a TRPA1 agonist was attenuated by pre-treatment with AP-18. Interpretation These results suggest trigeminovascular sensitization as a mechanism for enhanced headache susceptibility after chemical exposure.
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Li, Fengxian, Changxiong J. Guo, Cheng-Chiu Huang, Guang Yu, Sarah M. Brown, Shiyuan Xu, and Qin Liu. "Transient Receptor Potential A1 Activation Prolongs Isoflurane Induction Latency and Impairs Respiratory Function in Mice." Anesthesiology 122, no. 4 (April 1, 2015): 768–75. http://dx.doi.org/10.1097/aln.0000000000000607.

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Abstract Background: Isoflurane is a potent volatile anesthetic; however, it evokes airway irritation and neurogenic constriction through transient receptor potential (TRP) A1 channels and sensitizes TRPV1 channels, which colocalizes with TRPA1 in most of the vagal C-fibers innervating the airway. However, little is known about the precise effects of these two channels on the respiratory function during isoflurane anesthesia. Methods: By using a rodent behavioral model and whole-body plethysmograph, the authors examined the response of Trpa1−/− and Trpv1−/− mice to isoflurane anesthesia and monitored their respiratory functions during anesthesia. Results: This study showed that Trpa1−/− mice (n = 9), but not Trpv1−/− mice (n = 11), displayed a shortened induction latency compared with wild-type mice (n = 10) during isoflurane anesthesia (33 ± 2.0 s in wild-type and 33 ± 3.8 s in Trpv1−/−vs. 17 ± 1.8 in Trpa1−/− at 2.2 minimum alveolar concentrations). By contrast, their response to the nonpungent volatile anesthetic sevoflurane is indistinguishable from wild-type mice (24 ± 3.6 s in wild-type vs. 26 ± 1.0 s in Trpa1−/− at 2.4 minimum alveolar concentrations). The authors discovered that Trpa1−/− mice inhaled more anesthetic but maintained better respiratory function. Further respiration pattern analysis revealed that isoflurane triggered nociceptive reflexes and led to prolonged resting time between breaths during isoflurane induction as well as decreased dynamic pulmonary compliance, an indicator of airway constriction, throughout isoflurane anesthesia in wild-type and Trpv1−/− mice, but not in Trpa1−/− mice. Conclusion: Activation of TRPA1 by isoflurane negatively affects anesthetic induction latency by altering respiratory patterns and impairing pulmonary compliance.
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Zhou, Fangyuan, Katharina Metzner, Patrick Engel, Annika Balzulat, Marco Sisignano, Peter Ruth, Robert Lukowski, Achim Schmidtko, and Ruirui Lu. "Slack Potassium Channels Modulate TRPA1-Mediated Nociception in Sensory Neurons." Cells 11, no. 10 (May 19, 2022): 1693. http://dx.doi.org/10.3390/cells11101693.

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The transient receptor potential (TRP) ankyrin type 1 (TRPA1) channel is highly expressed in a subset of sensory neurons where it acts as an essential detector of painful stimuli. However, the mechanisms that control the activity of sensory neurons upon TRPA1 activation remain poorly understood. Here, using in situ hybridization and immunostaining, we found TRPA1 to be extensively co-localized with the potassium channel Slack (KNa1.1, Slo2.2, or Kcnt1) in sensory neurons. Mice lacking Slack globally (Slack−/−) or conditionally in sensory neurons (SNS-Slack−/−) demonstrated increased pain behavior after intraplantar injection of the TRPA1 activator allyl isothiocyanate. By contrast, pain behavior induced by the TRP vanilloid 1 (TRPV1) activator capsaicin was normal in Slack-deficient mice. Patch-clamp recordings in sensory neurons and in a HEK cell line transfected with TRPA1 and Slack revealed that Slack-dependent potassium currents (IKS) are modulated in a TRPA1-dependent manner. Taken together, our findings highlight Slack as a modulator of TRPA1-mediated, but not TRPV1-mediated, activation of sensory neurons.
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Hatano, Noriyuki, Hiroka Suzuki, Yukiko Muraki, and Katsuhiko Muraki. "Stimulation of human TRPA1 channels by clinical concentrations of the antirheumatic drug auranofin." American Journal of Physiology-Cell Physiology 304, no. 4 (February 15, 2013): C354—C361. http://dx.doi.org/10.1152/ajpcell.00096.2012.

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Gold compounds, which were widely used to treat rheumatoid arthritis, have been recently used as experimental agents for tumor treatment. Transient receptor potential (TRP) ankyrin repeat 1 (TRPA1) is a Ca2+-permeable ion channel that senses acute and inflammatory pain signals. Electrophilic compounds such as mustard oil and cinnamaldehyde activate TRPA1 by interacting with TRPA1 cysteine residues. Here we investigate the effects of the gold compound auranofin (AUR) on TRPA1 channels. Intracellular Ca2+ and whole cell patch-clamp recordings were performed on human embryonic kidney cells transiently expressed with TRPA1, TRP melastatin 8 (TRPM8), and vanilloid type TRP (TRPV1–4) channels. AUR stimulated TRPA1 in a concentration-dependent manner with a half-maximum potency of around 1.0 μM. The AUR-induced response was effectively blocked by HC030031, a TRPA1 antagonist. On the other hand, AUR failed to activate TRPM8 and TRPV1–4 channels, which are highly expressed in sensory neurons as nociceptors. The stimulatory effect on TRPA1 channels depended on the C414, C421, C621, and C633 cysteine residues and not on the inhibition of thioredoxin reductase by AUR. Moreover, AUR effectively activated TRPA1 channels expressed in human differentiated neuroblastoma cell lines. The study shows that AUR is a potent stimulator of TRPA1 channels.
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Dissertations / Theses on the topic "TRPA1"

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Hasan, S. M. Raquibul. "Modulation of the TRPA1 and TRPV1 ion channels." Thesis, University of Cambridge, 2014. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708079.

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Sinha, Sayantani. "Role of TRPA1 and TRPV1 in Propofol Induced Vasodilation." Thesis, Kent State University, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=3618926.

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Aims: Propofol, clinically named as Diprivan is an intravenous anesthetic known to cause hypotension in patients presenting for surgery. We have investigated the vasodilatory signaling cascade by which propofol causes hypotension using both in vivo and in vitro experimental approaches.

Methods and Results: Using high-fidelity microtip transducer catheter, mean arterial blood pressure (MAP) was measured in control, transient receptor potential ankyrin subtype 1 knock-out (TRPA1-/-), transient receptor potential vanilloid 1 knock-out (TRPV1-/-) and TRPA1-TRPV1 double-knockout mice (TRPAV-/-) in the presence and absence of L-NAME (an endothelial nitric oxide synthase inhibitor) and penitrem A [a big-conductance calcium gated (BKCa) channel inhibitor]. To further support our in-vivo data, murine coronary microvessels were isolated and cannulated for vasoreactivity studies. Furthermore, NO production from endothelial cells isolated from mouse aorta was also measured and immunocytochemical (ICC) studies were performed to show the intracellular localization of TRPA1 and TRPV1. Our in-vivo data shows that the characteristic propofol-induced depressor response is dependent on TRPA1-NO-BKCa pathway. Interestingly, vasoreactivity studies in isolated murine left anterior ascending (LAD) arteries demonstrate that TRPA1 and TRPV1 communicate with each other and propofol-induced vasodilation is dependent on both TRPA1 and TRPV1. Moreover our data also suggest that NO production and BK channel activation are the downstream mediators in this pathway. Finally, we demonstrate that NO production is attenuated in primary endothelial cells isolated from TRPAV-/- mice. ICC data also shows the co-localization of these channels in mouse aortic endothelial cells.

Conclusions: This is the first study which has shown that propofol-induced vasodilation involves TRPA1 in-vivo and also there is an implication of cross-talk between TRPA1 and TRPV1 in the coronary bed. Furthermore by understanding the mechanisms by which this anesthetic causes hypotension and coronary dilation will help to mitigate the potential harmful side-effects of anesthesia in patients with little cardiovascular reserve. This will in turn ensure a better and faster post-operative recovery in patients, especially benefiting those suffering from diabetes and other cardiovascular disorders.

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SINHA, SAYANTANI. "Role of TRPA1 and TRPV1 in Propofol Induced Vasodilation." Kent State University / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=kent1384901930.

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Sinharoy, Pritam. "Cross Talk Between TRPA1 and TRPV1 Ion-Channels: Role of Nitric Oxide." Kent State University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=kent1467381679.

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Sprague, Jared Michael. "TRPV1 Sensitization in Primary Sensory Neurons." Thesis, Harvard University, 2014. http://dissertations.umi.com/gsas.harvard:11441.

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Pain is a major personal and community burden throughout the world with currently limited treatment options for persistent pain due to unacceptable side effects, dependence or frank inefficacy. It is necessary to understand the anatomical and molecular pathways leading to pain to better cope with the current challenge of treating it.
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Fernandes, Maria Antionetta. "An investigation of the roles of TRPV1, TRPA1 and hydrogen sulfide in thermoregulation." Thesis, King's College London (University of London), 2015. http://kclpure.kcl.ac.uk/portal/en/theses/an-investigation-of-the-roles-of-trpv1-trpa1-and-hydrogen-sulfide-in-thermoregulation(811086d3-46c1-4f3f-9288-131bebf36431).html.

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The Transient Receptor Potential Vanilloid 1 (TRPV1) ion channel is an integrator of noxious stimuli, including noxious heat ( > 43°C), low pH ( < 6) and capsaicin (the pungent component of chilli peppers). Transient Receptor Potential Ankyrin 1 (TRPA1) is a closely related channel, activated by reactive oxygen species, hydrogen sulfide (H2S) and mustard oil. Their expression on primary sensory neurons is well characterised. Recent studies show that they are also expressed in non‐neuronal tissue. Whilst TRPV1 and TRPA1 antagonism is a promising analgesic and anti‐inflammatory strategy, early generation TRPV1 antagonists produced a poorly understood cross‐species side effect of hyperthermia. H2S is a vasodilator and TRPA1 activator. Inhalation of H2S can suspend animation, a state that includes a decreased body temperature. The role of TRPA1 and H2S in TRPV1‐mediated hyperthermia was investigated using TRPV1 and TRPA1 antagonists, knockout mice, H2S donors and modulators of endogenous H2S producing enzymes. The effects of TRPV1 antagonists SB366791 and JNJ17203212 and TRPA1 antagonists HC030031 and TCS5861528 on thermal and mechanical nociceptive thresholds of naïve mice were determined using the Hargreaves and automated Von Frey techniques, respectively. Antagonist‐induced changes in core body temperature of conscious, ambulatory mice were determined using radiotelemetry. Only JNJ17203212 produced a significant increase in core body temperature. The effects of the same antagonists on capsaicin‐ and mustard oil‐ induced blood flow changes in the pinna and knee were investigated, using full‐field laser Doppler perfusion. The capsaicin‐induced increase in pinna blood flow demonstrated a neuronal response; in the knee decreased flux demonstrated nonneuronal TRPV1 activation. Mustard oil similarly increased flux in the pinna and knee: TRPA1 does not exhibit any vasoconstrictor activity in this model. JNJ17203212 significantly attenuated capsaicin‐induced blood flow changes in the pinna and knee. No inhibition was observed with SB366791. HC030031 significantly reduced mustard oil‐induced blood flow increases in the pinna and knee whilst TCS5861528 had no effect. Finally, the involvement of TRPA1 blockade and H2S in JNJ17203212‐mediated hyperthermia was determined, using HC030031 and GYY4137, respectively. Whilst TRPA1 was not directly involved in our model, GYY4137 attenuated the hyperthermia elicited by JNJ17203212, suggesting H2S may have a role in TRPV1 antagonist‐mediated hyperthermia.
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Grace, Megan Stacey. "Investigating the role of TRPA1 and TRPV1 ion channels in the cough reflex." Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/14571.

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Cough is under the control of sensory afferents which innervate the airways via the vagus nerve. Cough is an important protective reflex that clears the airway, but can become exacerbated and deleterious when associated with airways diseases, in which there is enhanced release of inflammatory mediators and a decrease in lung pH. These mediators sensitise airway afferents and could be driving enhanced cough associated with inflammation. Transient Receptor Potential (TRP) ion channels are associated with several disease pathologies. TRPV1 has an established role in cough, and is implicated in the aetiology of chronic cough; and TRPA1 is a promising new target. Involvement of these ion channels in the tussive reflex is awaiting comprehensive investigation. I have therefore explored the role of TRPA1 and TRPV1 in tussive responses to the endogenous irritants prostaglandin E2 (PGE2), bradykinin (BK) and low pH. To do this I have used selective antagonists and genetically modified mice in models of human, guinea pig and mouse vagal sensory nerve depolarisation; conscious guinea pig cough; and guinea pig primary ganglia cell imaging. TRPA1 and TRPV1 were shown to mediate PGE2 and BK-induced nerve depolarisation, cough, and activation of ganglia cells. In contrast, low pH-induced nerve depolarisation and ganglia cell activation was mediated via TRPV1 or Acid Sensing Ion Channels (ASICs); whereas, cough was partially attenuated with TRPA1 or TRPV1 antagonists. In summary, I have identified that TRPA1 and TRPV1 mediate PGE2 and BK-induced cough; and provided evidence that low pH-induced sensory nerve activation is mediated via TRPV1 and ASICs, but a role for TRPA1 is still unclear. These are exciting findings which add to our understanding of the mechanisms that drive the cough reflex in the healthy state; builds a base for investigating cough hypersensitivity in disease; and could help to guide the development of novel efficacious anti-tussive therapies.
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Ibarra, Yessenia Michelle. "Characterization of human TRPA1 and TRPV1 channels in response to naturally occurring defensive compounds." Thesis, Harvard University, 2013. http://pqdtopen.proquest.com/#viewpdf?dispub=3566933.

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The transient receptor potential channels, ankyrin 1 (TRPA1) and vanilloid 1 (TRPV1), are non-selective cation-permeable channels that have retained their function as chemical sensors since their first appearance in metazoan species several hundred million years ago. In vertebrates, TRP channels have evolved multiple functions which make it difficult to understand exactly how they transmit signals to the brain that are interpreted very differently. For example, TRPA1 and TRPV1 are sensitive to various chemicals and activation of these channels produce sensations with opposing effects. Pain is felt when TRPV1 is activated by spider toxins, but activation by plant cannabidiol results in a pain-relieving sensation. Similarly, TRPA1 activation by delta-tetrahydrocannabinol is reported to relieve symptoms of pain, but TRPA1 activation by the active ingredient in wasabi results in a repulsive or noxious sensation. Much of what we know about TRPA1 and TRPV1 comes from the use of plant products or exposure to substances that cause or alleviate pain and inflammation. In this study, whole-cell voltage clamp recordings of heterologously expressed human TRPA1 and human TRPV1 were tested for sensitivity to a hallucinogenic plant compound, salvinorin A and an arthropod-defensive compound, para-benzoquinone. Neither compound has yet been reported to activate TRP channels but both are known to be involved in pain and inflammation signaling in humans. I show that the arthropod compound, para-benzoquinone, activates and desensitizes TRPA1 in a cysteine-dependent manner, but activation of TRPV1 is not dependent on cysteine reactivity. Although salvinorin A is known to be a potent agonist of the kappa-opioid and cannabinoid receptors, here I show that it also acts as a highly potent agonist of both TRPA1 and TRPV1. Its interaction with TRP channels may contribute to its antinociceptive effects in behavioral studies with animals that are reported to be independent of opioid signaling.

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DEMARTINI, CHIARA. "The role of TRPA1 and TRPV1 channels in trigeminal pain: data from animal models." Doctoral thesis, Università degli studi di Pavia, 2018. http://hdl.handle.net/11571/1214824.

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Experimental and clinical observations pointed out a critical involvement of transient receptor potential (TRP) channels, particularly TRPA1 and TRPV1, in trigeminal pain and associated symptoms, including hyperalgesia and allodynia. In this study the role of TRP channels was investigate in two animal models of diseases related to the trigeminal system: migraine and trigeminal neuropathic pain (TNP). TRPA1 and TRPV1 antagonists (ADM_12 and AMG9810 respectively) were used in the nitroglycerin (NTG)-induced hyperalgesia at the trigeminal level induced by means of the orofacial formalin test, a well validated animal model of migraine. The behavioral effects of AMG9810 gave inconclusive results, probably because its effect was confounded by the vehicle used. Nonetheless, it appears that TRPV1 channels are somehow involved in NTG-induced trigeminal hyperalgesia, since the TRPV1 mRNA levels were found to be strongly increased after NTG injection in medulla, cervical spinal cord and trigeminal ganglia (TG). NTG also up-regulated the mRNA levels of TRPA1, c-fos, calcitonin gene-related peptide (CGRP) and Substance P (SP) in the same areas. Those transcripts, but TRPV1, were reduced after ADM_12 treatment, which abolished the NTG-induced trigeminal hyperalgesia. The increased availability of nitric oxide after NTG promotes the formation of pro-inflammatory agents which can activate and/or sensitize nociceptors by means of TRPA1 and TRPV1 channels, causing the release of CGRP and SP. Although no differences in CGRP and SP protein expression were found at nucleus trigeminalis caudalis (NTC) level, the increased transcripts may reflect compensatory mechanisms aimed at reintegrating CGRP and SP stores depleted after NTG administration. It is possible that ADM_12 caused a reduction of Ca2+ influx through TRPA1 channels, which in turn interfered with the cascade of second-messenger molecules and with the Ca2+-interacting proteins, ultimately preventing NTG-induced inflammatory pathways. For TNP, the role of TRPA1 channels (by means of ADM_12) was investigated by evaluating mechanical allodynia in a model of chronic constriction injury of the infraorbital nerve (IoN-CCI). The IoN-CCI rats showed a hyperresponsiveness (4 weeks after surgery) at the ipsilateral side that reflects a condition of mechanical allodynia, and a significant increase in TRPA1, TRPV1, CGRP and SP mRNA expression levels. Although a tendency towards a decrease was seen in the ipsilateral compared to the contralateral side in the IoN-CCI rats, no significant differences in CGRP and SP protein expression at the NTC level were seen. However, their transcripts were highly increased in the central areas containing the NTC, as well as the TG ipsilateral to the IoN ligation. Both the allodynic response and the increased mRNA levels of operated rats were abolished after ADM_12 treatment. Probably, the blockade of TRPA1 channels located on the trigeminal afferents prevented neuropeptides release thus resulting in a reduced neurogenic inflammation and the nociceptors sensitization. Contrary to the migraine model, ADM_12 reduced transcript levels of both TRPs in IoN-CCI rats. Thus, ADM_12 appears to be a specific antagonist for TRPA1 in migraine pain, but in TNP it seems to act also on TRPV1. Probably, the damage induced by the nerve injury lead to a re-organization in expression and nature of the channels that made ADM_12 able to block TRPV1 channels. Since TRPA1 and TRPV1 are functionally linked, ADM_12 could have a direct effect on TRPA1 and an indirect effect on TRPV1 channels. In conclusion, TRPA1 blockade might be useful in the treatment of these trigeminal pain disorders. Moreover, our data suggest an important role also for TRPV1 channels, which could be differently involved depending on the type of pain. Further exploration on the mechanisms underlying the antinociceptive effects of these TRPs should improve our understanding of trigeminal pain processing.
Experimental and clinical observations pointed out a critical involvement of transient receptor potential (TRP) channels, particularly TRPA1 and TRPV1, in trigeminal pain and associated symptoms, including hyperalgesia and allodynia. In this study the role of TRP channels was investigate in two animal models of diseases related to the trigeminal system: migraine and trigeminal neuropathic pain (TNP). TRPA1 and TRPV1 antagonists (ADM_12 and AMG9810 respectively) were used in the nitroglycerin (NTG)-induced hyperalgesia at the trigeminal level induced by means of the orofacial formalin test, a well validated animal model of migraine. The behavioral effects of AMG9810 gave inconclusive results, probably because its effect was confounded by the vehicle used. Nonetheless, it appears that TRPV1 channels are somehow involved in NTG-induced trigeminal hyperalgesia, since the TRPV1 mRNA levels were found to be strongly increased after NTG injection in medulla, cervical spinal cord and trigeminal ganglia (TG). NTG also up-regulated the mRNA levels of TRPA1, c-fos, calcitonin gene-related peptide (CGRP) and Substance P (SP) in the same areas. Those transcripts, but TRPV1, were reduced after ADM_12 treatment, which abolished the NTG-induced trigeminal hyperalgesia. The increased availability of nitric oxide after NTG promotes the formation of pro-inflammatory agents which can activate and/or sensitize nociceptors by means of TRPA1 and TRPV1 channels, causing the release of CGRP and SP. Although no differences in CGRP and SP protein expression were found at nucleus trigeminalis caudalis (NTC) level, the increased transcripts may reflect compensatory mechanisms aimed at reintegrating CGRP and SP stores depleted after NTG administration. It is possible that ADM_12 caused a reduction of Ca2+ influx through TRPA1 channels, which in turn interfered with the cascade of second-messenger molecules and with the Ca2+-interacting proteins, ultimately preventing NTG-induced inflammatory pathways. For TNP, the role of TRPA1 channels (by means of ADM_12) was investigated by evaluating mechanical allodynia in a model of chronic constriction injury of the infraorbital nerve (IoN-CCI). The IoN-CCI rats showed a hyperresponsiveness (4 weeks after surgery) at the ipsilateral side that reflects a condition of mechanical allodynia, and a significant increase in TRPA1, TRPV1, CGRP and SP mRNA expression levels. Although a tendency towards a decrease was seen in the ipsilateral compared to the contralateral side in the IoN-CCI rats, no significant differences in CGRP and SP protein expression at the NTC level were seen. However, their transcripts were highly increased in the central areas containing the NTC, as well as the TG ipsilateral to the IoN ligation. Both the allodynic response and the increased mRNA levels of operated rats were abolished after ADM_12 treatment. Probably, the blockade of TRPA1 channels located on the trigeminal afferents prevented neuropeptides release thus resulting in a reduced neurogenic inflammation and the nociceptors sensitization. Contrary to the migraine model, ADM_12 reduced transcript levels of both TRPs in IoN-CCI rats. Thus, ADM_12 appears to be a specific antagonist for TRPA1 in migraine pain, but in TNP it seems to act also on TRPV1. Probably, the damage induced by the nerve injury lead to a re-organization in expression and nature of the channels that made ADM_12 able to block TRPV1 channels. Since TRPA1 and TRPV1 are functionally linked, ADM_12 could have a direct effect on TRPA1 and an indirect effect on TRPV1 channels. In conclusion, TRPA1 blockade might be useful in the treatment of these trigeminal pain disorders. Moreover, our data suggest an important role also for TRPV1 channels, which could be differently involved depending on the type of pain. Further exploration on the mechanisms underlying the antinociceptive effects of these TRPs should improve our understanding of trigeminal pain processing.
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Rosenzweig, Mark Ph D. Massachusetts Institute of Technology. "Drosophila TRPA1 controls thermotactic behavior." Thesis, Massachusetts Institute of Technology, 2006. http://hdl.handle.net/1721.1/34581.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2006.
Includes bibliographical references.
Temperature perception is an intricate process, essential for survival of many organisms. Temperatures far outside of the preferred range are usually harmful and are perceived as noxious (or painful), thus encouraging the animal to change its location or behavior. However, animals also have mechanisms to perceive more moderate, innocuous temperatures. Some animals exhibit clear directed movements in response to changes in temperature, a behavior known as thermotaxis. Thermotactic behavior has been most intensely studied in the nematode C. elegans, and a number of neurons and molecules that mediate thermotaxis in C. elegans have been identified. However, molecular mechanisms of temperature perception in general, and thermotaxis in particular, are still poorly understood. Drosophila melanogaster also exhibits strong temperature preferences and robust thermotactic behaviors, although the molecular mechanisms that mediate thermotaxis in Drosophila were unknown. We used a reverse genetic RNA interference (RNAi)-based strategy to identify Drosophila TRPA1 as a key regulator of thermotaxis. Larvae in which dTRPA1 expression has been knocked down with RNAi fail to avoid regions of moderately elevated temperature (~310C--350C).
(cont.) In heterologous cells, dTRPA1 protein is activated by warming (Viswanath, et al., 2003, Nature, 423:6942), suggesting that the role dTRPA1 plays in thermotaxis might be to sense the environmental temperature. We generated mutants in dTRPA1 using homologous recombination-mediated insertional mutagenesis. As expected, dtrpAl mutants were defective for thermotaxis at elevated temperatures, and surprisingly were also defective for thermotaxis at cold temperatures. Interestingly, dtrpAl mutants were not defective for avoidance of all cold temperatures, but the thermotactic defects of dtrpAl mutants were more pronounced at colder temperatures than at more moderate temperatures, suggesting that other mechanisms might compensate for the loss of dTRPA1 at more moderate temperatures. Temperature sensors were traditionally thought to be activated by and to mediate behavioral responses to restricted ranges of temperatures, either hot or cold temperatures, but not both. However, dTRPA1 appears to be required for thermotaxis behavior at both elevated and cold temperatures, raising an exciting possibility that dTRPA1 protein might mediate thermotaxis by serving as a sensor of both hot and cold temperatures.
(cont.) We also identified dTRPAl-expressing cells and implicated a subset of these cells in mediating thermotactic response to elevated temperatures. Surprisingly, our results suggest that the cells required for thermotaxis at elevated temperatures (dtrpAl-promoter-Gal4-expressing cells) are located in the larval central brain and not in the peripheral nervous system (PNS) where most thermal sensors are thought to function for mediating thermosensory behaviors. We further demonstrated that neither PAINLESS, a TRP channel required for proper larval responses to a high-temperature (38C--52C) nociceptive stimulus, nor the peripherally located neurons that mediatepainless behavior, were required for thermotaxis at elevated temperatures. On the other hand, dTRPA1 and the dtrpAl-promoter-Gal4-expressing central brain neurons that mediate thermotactic response to elevated temperatures appeared dispensable for larval responses to a high-temperature nociceptive stimulus. These findings suggest that different TRP channels and different neurons are used to mediate different thermosensory behaviors in Drosophila.
by Mark Rosenzweig.
Ph.D.
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Books on the topic "TRPA1"

1

Gomtsyan, Arthur, and Connie R. Faltynek, eds. Vanilloid Receptor TRPV1 in Drug Discovery. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2010. http://dx.doi.org/10.1002/9780470588284.

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Malmberg, Annika B., and Keith R. Bley, eds. Turning up the Heat on Pain: TRPV1 Receptors in Pain and Inflammation. Basel: Birkhäuser Basel, 2005. http://dx.doi.org/10.1007/3-7643-7379-2.

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Gomtsyan, Arthur. Vanilloid receptor TRPV1 in drug discovery: Targeting pain and other pathological disorders. Hoboken, N.J: Wiley, 2010.

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Gomtsyan, Arthur. Vanilloid receptor TRPV1 in drug discovery: Targeting pain and other pathological disorders. Hoboken, N.J: Wiley, 2010.

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Gomtsyan, Arthur, and Connie R. Faltynek. Vanilloid Receptor Trpv1 in Drug Discovery. Wiley & Sons, Incorporated, John, 2010.

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Sprague, Jared Michael. TRPV1 Sensitization in Primary Sensory Neurons. 2014.

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Li, Albert Steven. Structural studies of TRPV1 activation by capsaicin. 2009.

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Nagy, Istvan. VR1 in inflammatory thermal hyperalgesia. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0028.

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The landmark paper discussed in this chapter, published by Davis et al. in 2000, describes the role of the capsaicin receptor, which is called transient receptor potential cation channel subfamily vanilloid member 1 (TRPV1), in inflammatory thermal hyperalgesia. Capsaicin, the pungent agent found in hot peppers, has been linked to pain for centuries because it induces a burning pain sensation which, after prolonged application of the agent, turns into analgesia. Because of this, capsaicin has been used to relieve pain, most likely since prehistoric times. The elucidation of the role of TRPV1 in nociceptive processing was heralded as the starting point for the development of agents which would revolutionize pain management. Unfortunately, that promise is yet to be realized and apparently we need a more detailed understanding of the role of TRPV1 in physiological and pathological processes in order to fulfil the analgesic potential of drugs acting on this receptor.
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TRP01 - Royal Conservatory Technical Requirements for Piano Level 1 2015 Edition. The Frederick Harris Music Company, 2015.

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Vanilloid receptor TRPV1 in drug discovery: Targeting pain and other pathological disorders. Hoboken, N.J: Wiley, 2010.

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Book chapters on the topic "TRPA1"

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Zygmunt, Peter M., and Edward D. Högestätt. "TRPA1." In Handbook of Experimental Pharmacology, 583–630. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-54215-2_23.

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Zygmunt, Peter, and Edward Högestätt. "TRPA1 Channel." In Encyclopedia of Pain, 4092–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_4983.

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Chen, Jun, Steve McGaraughty, and Philip R. Kym. "TRPA1 in Drug Discovery." In Methods in Pharmacology and Toxicology, 43–59. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-077-9_3.

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Biswas-Fiss, Esther E., Stephanie Affet, Malissa Ha, Takaya Satoh, Joe B. Blumer, Stephen M. Lanier, Ana Kasirer-Friede, et al. "Ankyrine-Rich TRP Channel, ANKTM1, TRPA1." In Encyclopedia of Signaling Molecules, 113. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100063.

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De Logu, Francesco, Pierangelo Geppetti, and Romina Nassini. "Transient Receptor Potential Cation Channel Subfamily A Member 1 (TRPA1)." In Encyclopedia of Signaling Molecules, 5623–34. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101937.

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De Logu, Francesco, Pierangelo Geppetti, and Romina Nassini. "Transient Receptor Potential Cation Channel Subfamily A Member 1 (TRPA1)." In Encyclopedia of Signaling Molecules, 1–12. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4614-6438-9_101937-1.

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Nassini, Romina, Serena Materazzi, Silvia Benemei, and Pierangelo Geppetti. "The TRPA1 Channel in Inflammatory and Neuropathic Pain and Migraine." In Reviews of Physiology, Biochemistry and Pharmacology, 1–43. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/112_2014_18.

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Matassa, Danilo Swann, Ilenia Agliarulo, Maria Rosaria Amoroso, Rosario Avolio, Matteo Landriscina, and Franca Esposito. "TRAP1." In Encyclopedia of Signaling Molecules, 5680–90. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101888.

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Kon, Tetsuo, and Takahisa Furukawa. "TRPM1." In Encyclopedia of Signaling Molecules, 5727–34. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101948.

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Irie, Shoichi, and Takahisa Furukawa. "TRPM1." In Handbook of Experimental Pharmacology, 387–402. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-54215-2_15.

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Conference papers on the topic "TRPA1"

1

Dalenogare, Diéssica Padilha, Diulle Spat Peres, Maria Fernanda Pessano Fialho, and Gabriela Trevisan dos Santos. "Periorbital nociception in a progressive multiple sclerosis mouse model is dependent on TRPA1 channel activation." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.610.

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Background: Headache is one of the main painful symptoms described by multiple sclerosis patients. Previously, it was described that neuropathic pain-like behaviors were dependent on transient receptor potential ankyrin 1 (TRPA1) activation in a progressive multiple sclerosis model induced by experimental autoimmune encephalomyelitis (PMS- EAE) in mice. Objective: Here, we aimed to investigate if periorbital mechanical allodynia induced by PMS-EAE was also related to TRPA1 activation. Design and setting: Federal University of Santa Maria, Santa Maria, RS, Brazil. Methods: To induce a PMS-EAE we used female C57BL/6 wild-type and TRPA1- deficient (Trpa1-/-) mice. By the von Frey test, periorbital mechanical allodynia development was observed, and the nociception peak occurred 14 days after induction. At nociception peak day, the mice were treated with sumatriptan, TRPA1 antagonists (HC-030031, A-967079, metamizole, and propyphenazone. Results: The development of mechanical allodynia was showed as well as the antinociceptive effects for all treatments in induced mice. A significant reduction of TRPA1 expression was detected. Conclusion: Thus, these results suggest that headache-like symptoms induced by the PMS-EAE mouse model might occurring by TRPA1 activation.
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Grace, Megan S., Mark A. Birrell, Sarah A. Maher, and Maria G. Belvisi. "TRPA1 And TRPV1 Mediate Tussive Responses To PGE2, Bradykinin And Low PH." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5543.

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Maher, Sarah A., Megan S. Grace, Mark A. Birrell, and Maria G. Belvisi. "Prostaglandin E2-Induced Sensory Nerve Activation Is Mediated By TRPA1 And TRPV1." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5541.

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Li, F., and M. Wang. "The Role of TRPA1/TRPV1 in PM2.5 -Induced Airway Epithelial Cell Injury Model." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a7224.

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Moilanen, E. "SP0022 Trpa1 channels in osteoarthritis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.7275.

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Weisenburger, Sabrina, and MartinD Lehner. "Menthacarin® desensitizes TRPA1 channels." In GA – 69th Annual Meeting 2021, Virtual conference. Georg Thieme Verlag, 2021. http://dx.doi.org/10.1055/s-0041-1736939.

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Hazari, MS, N. Haykal-Coates, DW Winsett, AK Farraj, and DL Costa. "Acrolein Causes TRPA1-Mediated Sensory Irritation and Indirect Potentiation of TRPV1-Mediated Pulmonary Chemoreflex Response." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3152.

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Kotova, Olesya, Dina Gassan, Denis Naumov, and Juliy Perelman. "Effect of TRPA1 polymorphisms on asthma development." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa2345.

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Chen, Xue, Sara J. Bonvini, Eric Dubuis, Mark A. Birrell, and Maria G. Belvisi. "Characterisation of TRPA1 activation on sensory nerves." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa5263.

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Virk, H., E. Castells, V. Bowman, C. Feghali-Bostwick, Y. Amrani, P. Bradding, and Katy Roach. "TRPA1 ion channel expression in human lung myofibroblasts." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa1288.

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Reports on the topic "TRPA1"

1

Mohapatra, Durga P., Andrew Shepherd, and Lipin Loo. Therapeutic Targeting of TRPV1 for the Treatment of Chronic Pain Associated with Prostate Cancer Bone Metastasis. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada612310.

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Mohapatra, Durga P., Betty Diamond, Lipin Loo, and Andrew Shepherd. Therapeutic Targeting of TRPV1 for the Treatment of Chronic Pain Associated with Prostate Cancer Bone Metastasis. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada566497.

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Zuraw, Bruce L. Epithelial Cell TRPV1-Mediated Airway Sensitivity as a Mechanism for Respiratory Symptoms Associated with Gulf War Illness?". Fort Belvoir, VA: Defense Technical Information Center, June 2010. http://dx.doi.org/10.21236/ada536752.

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Buys, Michael J. Use of the TRPV1 Agonist Capsaicin to Provide Long-Term Analgesia in a Rat Limb Fracture/Open Repair, Internal Fixation Model. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada569521.

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Buys, Michael J. Use of the TRPV1 Agonist Capsaicin to Provide Long-Term Analgesia in a Rat Limb Fracture/Open Repair, Internal Fixation Model. Fort Belvoir, VA: Defense Technical Information Center, October 2011. http://dx.doi.org/10.21236/ada569523.

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