Relevant bibliographies by topics / TRPV1

Academic literature on the topic 'TRPV1'

Author: Grafiati
Published: 4 June 2021
Last updated: 14 March 2023

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Journal articles on the topic "TRPV1"

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Sharma, Deep, Rekha Rana, and Kiran Thakur. "A REVIEW ON ROLE OF TRPV CATION CHANNELS." Journal of Biomedical and Pharmaceutical Research 10, no. 2 (March 30, 2021): 32–51. http://dx.doi.org/10.32553/jbpr.v10i2.857.

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The mammalian branch of the Transient Receptor Potential (TRP) superfamily of cation channels consists of 28 members. They can be subdivided in six main subfamilies: the TRPC (‘Canonical’), TRPV (‘Vanilloid’), TRPM (‘Melastatin’), TRPP (‘Polycystin’), TRPML (‘Mucolipin’) and the TRPA (‘Ankyrin’) group. The TRPV subfamily comprises channels that are critically involved in nociception and thermo-sensing (TRPV1, TRPV2, TRPV3, TRPV4) as well as highly Ca2+ selective channels involved in Ca2+ absorption/ reabsorption in mammals (TRPV5, TRPV6). In this review we summarize fundamental physiological properties of all TRPV members in the light of various cellular functions of these channels and their significance in the various diseases.
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Chung, Gehoon, and Seog Bae Oh. "TRP Channels in Dental Pain." Open Pain Journal 6, no. 1 (March 8, 2013): 31–36. http://dx.doi.org/10.2174/1876386301306010031.

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Despite the high incidence of dental pain, the mechanism underlying its generation is mostly unknown. Functional expression of temperature-sensitive transient receptor potential (thermo-TRP) channels, such as TRPV1, TRPV2, TRPM8, and TRPA1 in dental primary afferent neurons and TRPV1, TRPV2, TRPV3, TRPV4, and TRPM3 in odontoblasts, has been demonstrated and suggested as responsible for dental pain elicited by hot and cold food. However, dental pain induced by light touch or sweet substance cannot be explained by the role of thermo-TRP channels. Most of current therapeutics of dentin hypersensitivity is based on hydrodynamic theory, which argues that light stimuli such as air puff and temperature changes cause fluid movement within dentinal tubule, which is then transduced as pain. To test this theory, various TRP channels as candidates of cellular mechanotransducers were studied for expression in dental primary afferents and odontoblasts. The expression of TRPV1, TRPV2, TRPA1, TRPV4, and TRPM3 in trigeminal neurons and TRPV1, TRPV2, TRPV3, TRPV4 and TRPM3 in odontoblasts has been revealed. However, their roles as cellular mechanotransducers are controversial and contribution to generation of dental pain is still elusive. This review discusses recent advances in understanding of molecular mechanism underlying development of dental pain.
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Marshall-Gradisnik, Sonya M., Peter Smith, Ekua W. Brenu, Bernd Nilius, Sandra B. Ramos, and Donald R. Staines. "Examination of Single Nucleotide Polymorphisms (SNPs) in Transient Receptor Potential (TRP) Ion Channels in Chronic Fatigue Syndrome Patients." Immunology and Immunogenetics Insights 7 (January 2015): III.S25147. http://dx.doi.org/10.4137/iii.s25147.

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Background The transient receptor potential (TRP) superfamily in humans comprises 27 cation channels with permeability to monovalent and divalent cations. These channels are widely expressed within humans on cells and tissues and have significant sensory and regulatory roles on most physiological functions. Chronic fatigue syndrome (CFS) is an unexplained disorder with multiple physiological impairments. OBJECTIVES The purpose of this study was to determine the role of TRPs in CFS. Methods The study comprised 115 CFS patients (age = 48.68 ± 1.06 years) and 90 nonfatigued controls (age = 46.48 ± 1.22 years). CFS patients were defined according to the 1994 Center for Disease Prevention and Control criteria for CFS. A total of 240 single nucleotide polymorphisms (SNPs) for 21 mammalian TRP ion channel genes ( TRPA1, TRPC1, TRPC2, TRPC3, TRPC4, TRPC6, TRPC7, TRPM1, TRPM2, TRPM3, TRPM4, TRPM5, TRPM6, TRPM7, TRPM8, TRPV1, TRPV2, TRPV3, TRPV4, TRPV5, and TRPV6) were examined via the Agena Biosciences iPLEX Gold assay. Statistical analysis was performed using the PLINK analysis software. Results Thirteen SNPs were significantly associated with CFS patients compared with the controls. Nine of these SNPs were associated with TRPM3 (rs12682832; P < 0.003, rs11142508; P < 0.004, rs1160742; P < 0.08, rs4454352; P < 0.013, rs1328153; P < 0.013, rs3763619; P < 0.014, rs7865858; P ≤ 0.021, rs1504401; P ≤ 0041, rs10115622; P ≤ 0.050), while the remainder were associated with TRPA1 (rs2383844; P ≤ 0.040, rs4738202; P ≤ 0.018) and TRPC4 (rs6650469; P ≤ 0.016, rs655207; P ≤ 0.018). Conclusion The data from this pilot study suggest an association between TRP ion channels, predominantly TRPM3 and CFS. This and other TRPs identified may contribute to the etiology and pathomechanism of CFS.
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Toledo Mauriño, Joel J., Gabriela Fonseca-Camarillo, Janette Furuzawa-Carballeda, Rafael Barreto-Zuñiga, Braulio Martínez Benítez, Julio Granados, and Jesus K. Yamamoto-Furusho. "TRPV Subfamily (TRPV2, TRPV3, TRPV4, TRPV5, and TRPV6) Gene and Protein Expression in Patients with Ulcerative Colitis." Journal of Immunology Research 2020 (May 8, 2020): 1–11. http://dx.doi.org/10.1155/2020/2906845.

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Introduction. TRPVs are a group of receptors with a channel activity predominantly permeable to Ca2+. This subfamily is involved in the development of gastrointestinal diseases such as ulcerative colitis (UC). The aim of the study was to characterize the gene and protein expression of the TRPV subfamily in UC patients and controls. Methods. We determined by quantitative PCR the gene expression of TRPV2, TRPV3, TRPV4, TRPV5, and TRPV6 in 45 UC patients (29 active UC and 16 remission UC) and 26 noninflamed controls. Protein expression was evaluated in 5 μm thick sections of formalin-fixed, paraffin-embedded tissue from 5 customized severe active UC patients and 5 control surgical specimens. Results. TRPV2 gene expression was increased in the control group compared with active UC and remission patients (P=0.002 and P=0.05, respectively). TRPV3 gene expression was significantly higher in controls than in active UC patients (P=0.002). The gene expression of TRPV4 was significantly higher in colonic tissue from patients with remission UC compared with active UC patients (P=0.05) and controls (P=0.005). TRPV5 had significantly higher mRNA levels in a control group compared with active UC patients (P=0.02). The gene expression of TRPV6 was significantly higher in the colonic tissue from patients with active UC compared with the control group (P=0.05). The protein expression of TRPV2 was upregulated in the mucosa and submucosa from the controls compared with the UC patients (P≤0.003). The protein expression of TRPV3 and TRPV4 was upregulated in all intestinal layers from the controls compared with the UC patients (P<0.001). TRPV5 was upregulated in the submucosa and serosa from the controls vs. UC patients (P<0.001). TRPV6 was upregulated in all intestinal layers from the UC patients vs. controls (P≤0.001). Conclusion. The TRPV subfamily clearly showed a differential expression in the UC patients compared with the controls, suggesting their role in the pathophysiology of UC.
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Kotova, O. O. "Modern concepts of the role of transient receptor potential channel vanilloid subfamily (TRPV) in development osmotic airway hyperresponsiveness in asthma patients (review)." Bulletin Physiology and Pathology of Respiration, no. 81 (September 29, 2021): 115–25. http://dx.doi.org/10.36604/1998-5029-2021-81-115-125.

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Introduction. Airway hyperresponsiveness to osmotic stimuli is often found among patients with asthma. It is assumed that the transient receptor potential channels of vanilloid subfamily (TRPV) may play a key role in the onset of this phenomenon.Aim. Review of modern world literature data on osmotic airway hyperresponsiveness and the role of TRPV channels in its development.Materials and methods. This review summarizes the data from articles published over the past five years found in PubMed and Google Scholar. However, earlier publications were also included if necessary.Results. The influence of natural osmotic triggers on the formation of bronchoconstriction in patients with asthma has been demonstrated. The effects that occur in the airways, depending on the functional state of TRPV1, TRPV2 and TRPV4 osmosensitive receptors are described, and the mechanisms that mediate the development of bronchial hyperresponsiveness with the participation of these channels are partially disclosed.Conclusion. It is safe to assume that TRPV channels are directly or indirectly associated with airway hyperresponsiveness to osmotic stimuli. Signaling cascades triggered by TRPV activation largely explain the effects of osmotic influence on the airways and the occurrence of bronchoconstriction. It could be suggested that TRPV1 signaling mediates the development of bronchospasm to hyperosmolar stimuli, while TRPV2 and TRPV4 are most likely involved in hypoosmotic-induced bronchoconstriction. Further study of the role of TRPV1, TRPV2 and TRPV4 in osmotic airway hyperresponsiveness is relevant and promising in terms of pharmacological management of this condition.
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Yang, Xiao-Ru, Mo-Jun Lin, Lionel S. McIntosh, and James S. K. Sham. "Functional expression of transient receptor potential melastatin- and vanilloid-related channels in pulmonary arterial and aortic smooth muscle." American Journal of Physiology-Lung Cellular and Molecular Physiology 290, no. 6 (June 2006): L1267—L1276. http://dx.doi.org/10.1152/ajplung.00515.2005.

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Transient receptor potential melastatin- (TRPM) and vanilloid-related (TRPV) channels are nonselective cation channels pertinent to diverse physiological functions. Multiple TRPM and TRPV channel subtypes have been identified and cloned in different tissues. However, their information in vascular tissue is scant. In this study, we sought to identify TRPM and TRPV channel subtypes expressed in rat deendothelialized intralobar pulmonary arteries (PAs) and aorta. With RT-PCR, mRNA of TRPM2, TRPM3, TRPM4, TRPM7, and TRPM8 of TRPM family and TRPV1, TRPV2, TRPV3, and TRPV4 of TRPV family were detected in both PAs and aorta. Quantitative real-time RT-PCR showed that TRPM8 and TRPV4 were the most abundantly expressed TRPM and TRPV subtypes, respectively. Moreover, Western blot analysis verified expression of TRPM2, TRPM8, TRPV1, and TRPV4 proteins in both types of vascular tissue. To examine the functional activities of these channels, we monitored intracellular Ca2+ transients ([Ca2+]i) in pulmonary arterial smooth muscle cells (PASMCs) and aortic smooth muscle cells (ASMCs). The TRPM8 agonist menthol (300 μM) and the TRPV4 agonist 4α-phorbol 12,13-didecanoate (1 μM) evoked significant increases in [Ca2+]i in PASMCs and ASMCs. These Ca2+ responses were abolished in the absence of extracellular Ca2+ or the presence of 300 μM Ni2+ but were unaffected by 1 μM nifedipine, suggesting Ca2+ influx via nonselective cation channels. Hence, for the first time, our results indicate that multiple functional TRPM and TRPV channels are coexpressed in rat intralobar PAs and aorta. These novel Ca2+ entry pathways may play important roles in the regulation of pulmonary and systemic circulation.
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Zhang, Lei, Sarahlouise Jones, Kate Brody, Marcello Costa, and Simon J. H. Brookes. "Thermosensitive transient receptor potential channels in vagal afferent neurons of the mouse." American Journal of Physiology-Gastrointestinal and Liver Physiology 286, no. 6 (June 2004): G983—G991. http://dx.doi.org/10.1152/ajpgi.00441.2003.

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A number of transient receptor potential (TRP) channels has recently been shown to mediate cutaneous thermosensitivity. Sensitivity to warm and cool stimuli has been demonstrated in both human and animal gastrointestinal tract; however, the molecular mechanisms that underlie this have not been determined. Vagal afferent neurons with cell bodies in the nodose ganglion are known to mediate nonnociceptive sensation from the upper gut. In this study, isolated cultured nodose ganglion from the mouse neurons showed changes in cytoplasmic-free Ca2+concentrations over a range of temperatures, as well as to icilin (a TRPM8 and TRPN1 agonist) and capsaicin (a TRPV1 agonist). RT-PCR was used to show the presence of six temperature-sensitive TRP channel transcripts (TRPV1–4, TRPN1, and TRPM8) in whole nodose ganglia. In addition, RT-PCR of single nodose cell bodies, which had been retrogradely labeled from the upper gut, detected transcripts for TRPV1, TRPV2, TRPV4, TRPN1, and TRPM8 in a proportion of cells. Immunohistochemical labeling detected TRPV1 and TRPV2 proteins in nodose ganglia. The presence of TRP channel transcripts and proteins was also detected in cells within several regions of the gastrointestinal tract. Our results reveal that TRP channels are present in subsets of vagal afferent neurons that project to the stomach and may confer temperature sensitivity on these cells.
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Peng, Gongyong, Wenju Lu, Xiaoyan Li, Yuqin Chen, Nanshan Zhong, Pixin Ran, and Jian Wang. "Expression of store-operated Ca2+ entry and transient receptor potential canonical and vanilloid-related proteins in rat distal pulmonary venous smooth muscle." American Journal of Physiology-Lung Cellular and Molecular Physiology 299, no. 5 (November 2010): L621—L630. http://dx.doi.org/10.1152/ajplung.00176.2009.

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Chronic hypoxia causes remodeling and alters contractile responses in both pulmonary arteries and pulmonary veins. Although pulmonary arteries have been studied extensively in these disorders, the mechanisms by which pulmonary veins respond to hypoxia and whether these responses contribute to chronic hypoxic pulmonary hypertension remain poorly understood. In pulmonary arterial smooth muscle, we have previously demonstrated that influx of Ca2+ through store-operated calcium channels (SOCC) thought to be composed of transient receptor potential (TRP) proteins is likely to play an important role in development of chronic hypoxic pulmonary hypertension. To determine whether this mechanism could also be operative in pulmonary venous smooth muscle, we measured intracellular Ca2+ concentration ([Ca2+]i) by fura-2 fluorescence microscopy in primary cultures of pulmonary venous smooth muscle cells (PVSMC) isolated from rat distal pulmonary veins. In cells perfused with Ca2+-free media containing cyclopiazonic acid (10 μM) and nifedipine (5 μM) to deplete sarcoplasmic reticulum Ca2+ stores and block voltage-dependent Ca2+ channels, restoration of extracellular Ca2+ (2.5 mM) caused marked increases in [Ca2+]i, whereas MnCl2 (200 μM) quenched fura-2 fluorescence, indicating store-operated Ca2+ entry (SOCE). SKF-96365 and NiCl2, antagonists of SOCC, blocked SOCE at concentrations that did not alter Ca2+ responses to 60 mM KCl. Of the seven known canonical TRP (TRPC1–7) and six vanilloid-related TRP channels (TRPV1–6), real-time PCR revealed mRNA expression of TRPC1 > TRPC6 > TRPC4 > TRPC2 ≈ TRPC5 > TRPC3, TRPV2 > TRPV4 > TRPV1 in distal PVSMC, and TRPC1 > TRPC6 > TRPC3 > TRPC4 ≈ TRPC5, TRPV2 ≈ TRPV4 > TRPV1 in rat distal pulmonary vein (PV) smooth muscle. Western blotting confirmed protein expression of TRPC1, TRPC6, TRPV2, and TRPV4 in both PVSMC and PV. Our results suggest that SOCE through Ca2+ channels composed of TRP proteins may contribute to Ca2+ signaling in rat distal PV smooth muscle.
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Kuwashima, Yutaro, Masataka Yanagawa, Mitsuhiro Abe, Michio Hiroshima, Masahiro Ueda, Makoto Arita, and Yasushi Sako. "Comparative Analysis of Single-Molecule Dynamics of TRPV1 and TRPV4 Channels in Living Cells." International Journal of Molecular Sciences 22, no. 16 (August 6, 2021): 8473. http://dx.doi.org/10.3390/ijms22168473.

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TRPV1 and TRPV4, members of the transient receptor potential vanilloid family, are multimodal ion channels activated by various stimuli, including temperature and chemicals. It has been demonstrated that TRPV channels function as tetramers; however, the dynamics of the diffusion, oligomerization, and endocytosis of these channels in living cells are unclear. Here we undertook single-molecule time-lapse imaging of TRPV1 and TRPV4 in HEK 293 cells. Differences were observed between TRPV1 and TRPV4 before and after agonist stimulation. In the resting state, TRPV4 was more likely to form higher-order oligomers within immobile membrane domains than TRPV1. TRPV1 became immobile after capsaicin stimulation, followed by its gradual endocytosis. In contrast, TRPV4 was rapidly internalized upon stimulation with GSK1016790A. The selective loss of immobile higher-order oligomers from the cell surface through endocytosis increased the proportion of the fast-diffusing state for both subtypes. With the increase in the fast state, the association rate constants of TRPV1 and TRPV4 increased, regenerating the higher-order oligomers. Our results provide a possible mechanism for the different rates of endocytosis of TRPV1 and TRPV4 based on the spatial organization of the higher-order structures of the two TRPV channels.
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Yoo, Hae Young, Su Jung Park, Eun-Young Seo, Kyung Sun Park, Jung-A. Han, Kyung Soo Kim, Dong Hoon Shin, Yung E. Earm, Yin-Hua Zhang, and Sung Joon Kim. "Role of thromboxane A2-activated nonselective cation channels in hypoxic pulmonary vasoconstriction of rat." American Journal of Physiology-Cell Physiology 302, no. 1 (January 2012): C307—C317. http://dx.doi.org/10.1152/ajpcell.00153.2011.

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Hypoxia-induced pulmonary vasoconstriction (HPV) is critical for matching of ventilation/perfusion in lungs. Although hypoxic inhibition of K+ channels has been a leading hypothesis for depolarization of pulmonary arterial smooth muscle cells (PASMCs) under hypoxia, pharmacological inhibition of K+ channels does not induce significant contraction in rat pulmonary arteries. Because a partial contraction by thromboxane A2 (TXA2) is required for induction of HPV, we hypothesize that TXA2 receptor (TP) stimulation might activate depolarizing nonselective cation channels (NSCs). Consistently, we found that 5–10 nM U46619, a stable agonist for TP, was indispensible for contraction of rat pulmonary arteries by 4-aminopyridine, a blocker of voltage-gated K+ channel (Kv). Whole cell voltage clamp with rat PASMC revealed that U46619 induced a NSC current ( INSC,TXA2) with weakly outward rectifying current-voltage relation. INSC,TXA2 was blocked by ruthenium red (RR), an antagonist of the transient receptor potential vanilloid-related channel (TRPV) subfamily. 2-Aminoethoxydiphenyl borate, an agonist for TRPV1–3, consistently activated NSC channels in PASMCs. In contrast, agonists for TRPV1 (capsaicin), TRPV3 (camphor), or TRPV4 (α-PDD) rarely induced an increase in the membrane conductance of PASMCs. RT-PCR analysis showed the expression of transcripts for TRPV2 and -4 in rat PASMCs. Finally, it was confirmed that pretreatment with RR largely inhibited HPV in the presence of U46619. The pretreatment with agonists for TRPV1 (capsaicin) and TRPV4 (α-PDD) was ineffective as pretone agents for HPV. Taken together, it is suggested that the concerted effects of INSC,TXA2 activation and Kv inhibition under hypoxia induce membrane depolarization sufficient for HPV. TRPV2 is carefully suggested as the TXA2-activated NSC in rat PASMC.
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Dissertations / Theses on the topic "TRPV1"

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Hering, Nils [Verfasser]. "Elektrophysiologische Charakterisierung der Ionenkanäle TRPV1, TRPV3 und TRPV4 exprimiert in Xenopus Oozyten. / Nils Hering." Kiel : Universitätsbibliothek Kiel, 2016. http://d-nb.info/1096220881/34.

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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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Hellwig, Nicole. "Protonenleitfähigkeit von TRPV1 und Multimerisierung von TRPV-Kanaluntereinheiten." [S.l.] : [s.n.], 2005. http://www.diss.fu-berlin.de/2005/177/index.html.

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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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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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O'Leary, Caitriona. "The role of TRPV1 and TRPV4 channels in retinal angiogenesis." Thesis, Queen's University Belfast, 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709849.

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Abnormal angiogenesis is a key pathological process associated with many diseases such as metastatic cancer, atherosclerosis, and sight-threatening disorders including proliferative diabetic retinopathy, neovascular age-related macular degeneration, and retinopathy of prematurity. Calcium signalling is fundamental for many endothelial functions including the regulation of blood vessel tone, barrier selectivity and angiogenesis. Calcium influx has been implicated in retinal endothelial cell angiogenic response, but the molecular identity of the underlying calcium channels remains to be fully elucidated. In the present study we have investigated the role of the calcium permeable channels TRPV1 and TRPV4 in retinal angiogenesis both in vitro an in vivo. Both mRNA and protein expression of TRPV1 and TRPV4 were initially confirmed in RMECs using PCR and western blotting experiments, functional channel expression was confirmed using whole cell patch clamp techniques. Pharmacological inhibition of TRPV1 and TRPV4 channels reduced angiogenesis in vitro via modulation of tubulogenesis. HGF-stimulated angiogenesis was found to be sensitive to both TRPV1 and TRPV4 inhibition, but channel inhibition had no effect on VEGF or FGF stimulated angiogenesis in vitro. Inhibition of both channels in vivo reduced hypoxia-dependent retinal neovascularisation and promoted normal therapeutic angiogenesis in an oxygen-induced retinopathy mouse model. TRPV1 inhibition was found to downregulate the mRNA expression of TNF-alpha in vivo, whilst TRPV4 inhibition had no effect. TRPV1 and TRPV4 channels were also found to form functional heterotetrameric channels in retinal endothelial cells in vitro. This study provides evidence for TRPV1 and TRPV4 channels as effective therapeutic targets in retinal angiogenesis both in vitro and in vivo.
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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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Chen, Lan [Verfasser]. "Functional TRPV1 and TRPV4 channels in the murine renal vasculature / Lan Chen." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2017. http://d-nb.info/1148425926/34.

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SUGIHARA, YASUO, MINORU UEDA, HIDEYUKI NAKASHIMA, KENJIRO NAGAMINE, HISASHI HATTORI, NORIYUKI OZAKI, and KATSUNORI HIRONAKA. "INVOLVEMENT OF GLIAL ACTIVATION IN TRIGEMINAL GANGLION IN A RAT MODEL OF LOWER GINGIVAL CANCER PAIN." Nagoya University School of Medicine, 2014. http://hdl.handle.net/2237/20551.

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Books on the topic "TRPV1"

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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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McGoldrick, Luke Lawrence Reedy. Structural Analyses of the Transient Receptor Potential Channels TRPV3 and TRPV6. [New York, N.Y.?]: [publisher not identified], 2019.

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Doyle, Christina. Functional Characterization of the Mammalian TRPV4 Channel: Yeast Screen Reveals Gain-of-Function Mutations. [New York, N.Y.?]: [publisher not identified], 2012.

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Liu, Shu. Temperature- and touch-sensitive neurons couple CNG and TRPV channel activities to control heat avoidance in Caenorhabditis elegans. Freiburg: Universität, 2012.

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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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Book chapters on the topic "TRPV1"

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Zhu, Michael X. "Transient Receptor Potential Channels TRPV1, TRPV2, and TRPV3." In Encyclopedia of Metalloproteins, 2253–57. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-1533-6_441.

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Bevan, Stuart, Talisia Quallo, and David A. Andersson. "TRPV1." In Handbook of Experimental Pharmacology, 207–45. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-54215-2_9.

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Winter, Janet. "TRPV1 distribution and regulation." In Turning up the Heat on Pain: TRPV1 Receptors in Pain and Inflammation, 39–51. Basel: Birkhäuser Basel, 2005. http://dx.doi.org/10.1007/3-7643-7379-2_3.

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Belvisi, Maria G., and Peter J. Barnes. "TRPV1 in the airways." In Turning up the Heat on Pain: TRPV1 Receptors in Pain and Inflammation, 167–87. Basel: Birkhäuser Basel, 2005. http://dx.doi.org/10.1007/3-7643-7379-2_9.

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McNaughton, Peter A. "TRPV1 Modulation by PKC." In Encyclopedia of Pain, 4102–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_4645.

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McIntyre, Peter. "TRPV1 Receptor, Species Variability." In Encyclopedia of Pain, 4104–9. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_4650.

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Jordt, Sven-Eric. "TRPV1, Regulation by Protons." In Encyclopedia of Pain, 4112–15. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_4653.

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Valenzano, Kenneth J., James D. Pomonis, and Katharine Walker. "TRPV1 antagonists and chronic pain." In Turning up the Heat on Pain: TRPV1 Receptors in Pain and Inflammation, 227–43. Basel: Birkhäuser Basel, 2005. http://dx.doi.org/10.1007/3-7643-7379-2_12.

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Tominaga, Makoto. "Structural determinants of TRPV1 functionality." In Turning up the Heat on Pain: TRPV1 Receptors in Pain and Inflammation, 25–37. Basel: Birkhäuser Basel, 2005. http://dx.doi.org/10.1007/3-7643-7379-2_2.

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Moriello, Aniello Schiano, and Luciano De Petrocellis. "Assay of TRPV1 Receptor Signaling." In Methods in Molecular Biology, 65–76. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3539-0_7.

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Conference papers on the topic "TRPV1"

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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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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, Denis Naumov, Anna Prikhodko, Juliy Perelman, and Victor Kolosov. "TRPV1 and TRPV2 are up-regulated in the airways of asthma patients with osmotic airway hyperresponsiveness." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa1820.

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Sahebari, M., SZ Mirfeizi, and J. Salimi. "PS1:14 Trpv1 receptor activity in lupus." In 11th European Lupus Meeting, Düsseldorf, Germany, 21–24 March 2018, Abstract presentations. Lupus Foundation of America, 2018. http://dx.doi.org/10.1136/lupus-2018-abstract.62.

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Suh, Eul, Agnella Izzo Matic, Margarete Otting, Joseph T. Walsh, Jr., and Claus-Peter Richter. "Optical stimulation in mice lacking the TRPV1 channel." In SPIE BiOS: Biomedical Optics, edited by Anita Mahadevan-Jansen and E. Duco Jansen. SPIE, 2009. http://dx.doi.org/10.1117/12.816891.

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Duarte, AG, GA Campbell, and AC Myers. "Quantitative Assessment of TRPV1 in Lung Transplant Recipients." 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.a6052.

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Jendzjowsky, N., A. Roy, and R. Wilson. "Th2 Cytokines Stimulate Carotid Body Chemoreceptors via TRPV1 Channels." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5603.

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Grandes Moreno, Pedro, Izaskun Elezgarai Gabantxo, Inmaculada Gerrikagoitia Marina, Nagore Puente Bustinza, Juan Luis Mendizabal Zubiaga, Itziar Terradillos Irastorza, Irantzu Rico Barrio, and Jon Egaña Huguet. "TRPV1-KO saguek epilepsia krisi arinagoak jasatearen zergatiak bilatzen." In II. Ikergazte. Nazioarteko ikerketa euskaraz. Bilbao: UEU arg, 2017. http://dx.doi.org/10.26876/ikergazte.ii.04.10.

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Reports on the topic "TRPV1"

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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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