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Pesquisa : D12.776.157.530.400.901.250 [Categoria DeCS]
Referências encontradas : 925 [refinar]
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[PMID]:29254302
[Au] Autor:Wang Q; Wang J; Gao D; Li J
[Ad] Endereço:Tumor Center, The First Hospital of Jilin University, Changchun, Jilin, China.
[Ti] Título:Inhibition of PAR2 and TRPA1 signals alleviates neuropathic pain evoked by chemotherapeutic bortezomib.
[So] Source:J Biol Regul Homeost Agents;31(4):977-983, 2017 Oct-Dec.
[Is] ISSN:0393-974X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:Bortezomib (BTZ) is generally used as a chemotherapeutic agent for the treatment of multiple myeloma; however, one of the significant limiting complications of BTZ is painful peripheral neuropathy observed during BTZ therapy. There is a lack of drugs which can prevent and/or treat the painful symptoms induced by BTZ, as the underlying molecular mechanism leading to neuropathic pain remains largely unclear. In the present study, we examined engagement of proteinase-activated receptor 2 (PAR2) and transient receptor potential ankyrin 1 (TRPA1) in neuropathic pain induced by BTZ in rats. Our results demonstrated that systemic injection of BTZ increased mechanical pain and cold sensitivity as compared with control animals (P less than 0.05 vs control rats). Our data further showed that blocking respective PAR2 and TRPA1 attenuated mechanical pain and cold sensitivity observed in control rats and BTZ rats (P less than 0.05 vs vehicle control). Notably, the attenuating effect of blocking PAR2 and TRPA1 on mechanical pain and cold sensitivity was significantly less in BTZ rats than that in control rats. In addition, protein expression of PAR2 and TRPA1 was upregulated in the lumbar dorsal root ganglion of BTZ rats, and inhibition of PAR2 decreased the levels of TRPA1 and attenuated its downstream pathways (namely, PKCÉ› and PKA). Overall, we revealed specific signaling pathways leading to neuropathic pain induced by chemotherapeutic BTZ and that blocking PAR2 and TRPA1 in sensory nerves is beneficial to improve neuropathic pain during BTZ intervention.
[Mh] Termos MeSH primário: Analgésicos/farmacologia
Antineoplásicos/efeitos adversos
Bortezomib/efeitos adversos
Neuralgia/prevenção & controle
Oligopeptídeos/farmacologia
Receptor PAR-2/antagonistas & inibidores
Canal de Cátion TRPA1/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Proteínas Quinases Dependentes de AMP Cíclico/genética
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
Gânglios Espinais/efeitos dos fármacos
Gânglios Espinais/metabolismo
Gânglios Espinais/fisiopatologia
Regulação da Expressão Gênica
Hiperalgesia/induzido quimicamente
Hiperalgesia/genética
Hiperalgesia/fisiopatologia
Hiperalgesia/prevenção & controle
Masculino
Neuralgia/induzido quimicamente
Neuralgia/genética
Neuralgia/fisiopatologia
Proteína Quinase C-épsilon/genética
Proteína Quinase C-épsilon/metabolismo
Ratos
Ratos Sprague-Dawley
Receptor PAR-2/genética
Receptor PAR-2/metabolismo
Transdução de Sinais
Canal de Cátion TRPA1/genética
Canal de Cátion TRPA1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Analgesics); 0 (Antineoplastic Agents); 0 (H-Phe-Ser-Leu-Leu-Arg-Tyr-NH2); 0 (Oligopeptides); 0 (Receptor, PAR-2); 0 (TRPA1 Cation Channel); 0 (Trpa1 protein, rat); 69G8BD63PP (Bortezomib); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); EC 2.7.11.13 (Protein Kinase C-epsilon)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE


  2 / 925 MEDLINE  
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[PMID]:28468269
[Au] Autor:Logashina YA; Solstad RG; Mineev KS; Korolkova YV; Mosharova IV; Dyachenko IA; Palikov VA; Palikova YA; Murashev AN; Arseniev AS; Kozlov SA; Stensvåg K; Haug T; Andreev YA
[Ad] Endereço:Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, ul. Miklukho-Maklaya 16/10, 117997 Moscow, Russia. yulia.logashina@gmail.com.
[Ti] Título:New Disulfide-Stabilized Fold Provides Sea Anemone Peptide to Exhibit Both Antimicrobial and TRPA1 Potentiating Properties.
[So] Source:Toxins (Basel);9(5), 2017 Apr 29.
[Is] ISSN:2072-6651
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:A novel bioactive peptide named τ-AnmTx Ueq 12-1 (short name Ueq 12-1) was isolated and characterized from the sea anemone Ueq 12-1 is unique among the variety of known sea anemone peptides in terms of its primary and spatial structure. It consists of 45 amino acids including 10 cysteine residues with an unusual distribution and represents a new group of sea anemone peptides. The 3D structure of Ueq 12-1, determined by NMR spectroscopy, represents a new disulfide-stabilized fold partly similar to the defensin-like fold. Ueq 12-1 showed the dual activity of both a moderate antibacterial activity against Gram-positive bacteria and a potentiating activity on the transient receptor potential ankyrin 1 (TRPA1). Ueq 12-1 is a unique peptide potentiator of the TRPA1 receptor that produces analgesic and anti-inflammatory effects . The antinociceptive properties allow us to consider Ueq 12-1 as a potential analgesic drug lead with antibacterial properties.
[Mh] Termos MeSH primário: Analgésicos
Antibacterianos
Anti-Inflamatórios
Peptídeos
Anêmonas-do-Mar
Canal de Cátion TRPA1/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Analgésicos/química
Analgésicos/isolamento & purificação
Analgésicos/farmacologia
Analgésicos/uso terapêutico
Animais
Antibacterianos/química
Antibacterianos/isolamento & purificação
Antibacterianos/farmacologia
Antibacterianos/uso terapêutico
Anti-Inflamatórios/química
Anti-Inflamatórios/isolamento & purificação
Anti-Inflamatórios/farmacologia
Anti-Inflamatórios/uso terapêutico
Dissulfetos/química
Edema/tratamento farmacológico
Peptídeos/química
Peptídeos/isolamento & purificação
Peptídeos/farmacologia
Peptídeos/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Analgesics); 0 (Anti-Bacterial Agents); 0 (Anti-Inflammatory Agents); 0 (Disulfides); 0 (Peptides); 0 (TRPA1 Cation Channel)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE


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[PMID]:29198882
[Au] Autor:Sekiguchi K; Ogawa E; Kurohane K; Konishi H; Mochizuki N; Manabe K; Imai Y
[Ad] Endereço:Laboratory of Microbiology and Immunology, School of Pharmaceutical Sciences, University of Shizuoka, 52-1 Yada, Suruga-ku, Shizuoka City, Shizuoka 422-8526, Japan.
[Ti] Título:Adjuvant effect of short chain triacylglycerol tributyrin on a mouse contact hypersensitivity model.
[So] Source:Toxicol Lett;284:56-62, 2018 Mar 01.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Little attention has been paid to chemicals that can enhance hypersensitivity caused by other chemicals. We have demonstrated that phthalate esters with short chain alcohols enhance fluorescein isothiocyanate (FITC)-induced contact hypersensitivity (CHS) in a mouse model. Furthermore, phthalate esters with such an enhancing effect were found to activate transient receptor potential ankyrin 1 (TRPA1) cation channels, which are expressed on a part of sensory neurons, using a TRPA1-expressing cell line. In this study, we examined these activities of esters comprising glycerol and a short chain fatty acid, i.e. dibutyrin and tributyrin. We carried out chemical synthesis of dibutyrin isomers. Each dibutyrin isomer weakly activated TRPA1 and slightly enhanced skin sensitization to FITC. Unexpectedly, TRPA1 activation and enhancement of FITC-CHS were much more evident in the presence of tributyrin. Mechanistically, tributyrin induced increased dendritic cell trafficking from the skin to draining lymph nodes. Tributyrin enhanced interferon-γ (IFN-γ) production by draining lymph nodes, while its effect on interleukin-4 (IL-4) production was relatively less prominent. These results suggested that tributyrin concomitantly caused TRPA1 activation and an adjuvant effect on FITC-CHS.
[Mh] Termos MeSH primário: Adjuvantes Imunológicos/toxicidade
Dermatite de Contato/imunologia
Canal de Cátion TRPA1/metabolismo
Triglicerídeos/toxicidade
[Mh] Termos MeSH secundário: Adjuvantes Imunológicos/administração & dosagem
Animais
Células CHO
Movimento Celular/efeitos dos fármacos
Cricetulus
Células Dendríticas/efeitos dos fármacos
Dermatite de Contato/metabolismo
Modelos Animais de Doenças
Feminino
Fluoresceína-5-Isotiocianato/administração & dosagem
Fluoresceína-5-Isotiocianato/toxicidade
Seres Humanos
Interferon gama/metabolismo
Interleucina-4/metabolismo
Linfonodos/efeitos dos fármacos
Linfonodos/imunologia
Camundongos Endogâmicos BALB C
Pele/efeitos dos fármacos
Pele/imunologia
Triglicerídeos/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adjuvants, Immunologic); 0 (TRPA1 Cation Channel); 0 (Triglycerides); 207137-56-2 (Interleukin-4); 82115-62-6 (Interferon-gamma); I223NX31W9 (Fluorescein-5-isothiocyanate); S05LZ624MF (tributyrin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE


  4 / 925 MEDLINE  
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[PMID]:29184198
[Au] Autor:Arenas OM; Zaharieva EE; Para A; Vásquez-Doorman C; Petersen CP; Gallio M
[Ad] Endereço:Department of Neurobiology, Northwestern University, Evanston, IL, USA.
[Ti] Título:Activation of planarian TRPA1 by reactive oxygen species reveals a conserved mechanism for animal nociception.
[So] Source:Nat Neurosci;20(12):1686-1693, 2017 Dec.
[Is] ISSN:1546-1726
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:All animals must detect noxious stimuli to initiate protective behavior, but the evolutionary origin of nociceptive systems is not well understood. Here we show that noxious heat and irritant chemicals elicit robust escape behaviors in the planarian Schmidtea mediterranea and that the conserved ion channel TRPA1 is required for these responses. TRPA1-mutant Drosophila flies are also defective in noxious-heat responses. We find that either planarian or human TRPA1 can restore noxious-heat avoidance to TRPA1-mutant Drosophila, although neither is directly activated by heat. Instead, our data suggest that TRPA1 activation is mediated by H O and reactive oxygen species, early markers of tissue damage rapidly produced as a result of heat exposure. Together, our data reveal a core function for TRPA1 in noxious heat transduction, demonstrate its conservation from planarians to humans, and imply that animal nociceptive systems may share a common ancestry, tracing back to a progenitor that lived more than 500 million years ago.
[Mh] Termos MeSH primário: Nociceptividade/fisiologia
Planárias/fisiologia
Espécies Reativas de Oxigênio/farmacologia
Canal de Cátion TRPA1/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Aprendizagem da Esquiva/efeitos dos fármacos
Comportamento Animal/efeitos dos fármacos
Drosophila
Proteínas de Drosophila/genética
Peróxido de Hidrogênio/farmacologia
Nociceptividade/efeitos dos fármacos
Técnicas de Patch-Clamp
Interferência de RNA
Canal de Cátion TRPA1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drosophila Proteins); 0 (Reactive Oxygen Species); 0 (TRPA1 Cation Channel); 0 (TRPA1 protein, human); 0 (TrpA1 protein, Drosophila); BBX060AN9V (Hydrogen Peroxide)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171219
[Lr] Data última revisão:
171219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE
[do] DOI:10.1038/s41593-017-0005-0


  5 / 925 MEDLINE  
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[PMID]:28903060
[Au] Autor:Nalli M; Ortar G; Schiano Moriello A; Di Marzo V; De Petrocellis L
[Ad] Endereço:Dipartimento di Chimica e Tecnologie del Farmaco, Sapienza Università di Roma, piazzale Aldo Moro 5, 00185 Roma, Italy. Electronic address: marianna.nalli@uniroma1.it.
[Ti] Título:Effects of curcumin and curcumin analogues on TRP channels.
[So] Source:Fitoterapia;122:126-131, 2017 Oct.
[Is] ISSN:1873-6971
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:A series of 33 curcumin analogues was synthesized and tested on TRPA1, TRPM8, and TRPV1 channels. Twenty of them acted as good modulators of TRPA1 channels. None was able to significantly activate TRPM8 channels, while curcumin itself and six curcuminoids belonging to the 1,3-dicarbonyl and acyclic series behaved as 'true' antagonists with IC values<5µM. Only few curcuminoids were able to modulate TRPV1 channels with EC and IC values ranging from 3.4 and 6.0µM.
[Mh] Termos MeSH primário: Curcumina/análogos & derivados
Canais de Receptores Transientes de Potencial/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Células HEK293
Seres Humanos
Estrutura Molecular
Ratos
Canal de Cátion TRPA1
Canais de Cátion TRPC/efeitos dos fármacos
Canais de Cátion TRPM/efeitos dos fármacos
Canais de Cátion TRPV/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (TRPA1 Cation Channel); 0 (TRPC Cation Channels); 0 (TRPM Cation Channels); 0 (TRPV Cation Channels); 0 (TRPV1 protein, human); 0 (Transient Receptor Potential Channels); 0 (Trpa1 protein, rat); 0 (Trpm8 protein, rat); IT942ZTH98 (Curcumin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170914
[St] Status:MEDLINE


  6 / 925 MEDLINE  
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[PMID]:28657737
[Au] Autor:Mathie K; Lainer J; Spreng S; Dawid C; Andersson DA; Bevan S; Hofmann T
[Ad] Endereço:Chair of Food Chemistry and Molecular Sensory Science, Technische Universität München , Lise-Meitner-Straße 34, D-85350 Freising, Germany , and.
[Ti] Título:Structure-Pungency Relationships and TRP Channel Activation of Drimane Sesquiterpenes in Tasmanian Pepper (Tasmannia lanceolata).
[So] Source:J Agric Food Chem;65(28):5700-5712, 2017 Jul 19.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sensory-guided fractionation of extracts of Tasmanian pepper berries revealed 20 drimane sesquiterpens, among which polygodial, warburganal, and 1ß-acetoxy-9-deoxy-isomuzigadial exhibited the lowest pungency threshold concentrations on the tongue surface (0.6-2.8 nmol/cm ) and elicited a dose-dependent calcium influx into mTRPA1 expressing CHO cells with the lowest EC values (4.5 ± 1.0 to 16.7 ± 7.5 µmol/L) and a good correlation to oral pungency thresholds (R = 0.986, linear regression). Calcium imaging assays demonstrated these chemosensates to induce a calcium influx into cultured trigeminal neurons prepared from wildtype (TRPA1 ) mice, whereas no calcium influx was observed in neurons from TRPA1 knockout mice (TRPA1 ), thus confirming the α,ß-unsaturated 1,4-dialdehyde structure to be the required structural motif for a low oral puncency thresholds and activation of the Transient Receptor Potential Channel A1 (TRPA1). Time-resolved NMR experiments confirmed the pungency mediating mechanism for electrophilic drimane sesquiterpene dialdehydes to be different from that found for other electrophilic pungent agents like isothiocyanates, which have been shown to undergo a covalent binding with cysteine residues in TRPA1. Instead, the high-impact chemosensates polygodial, warburganal, and 1ß-acetoxy-9-deoxy-isomuzigadial showed immediate reactivity with the ε-amino group of lysine side chains to give pyrrole-type conjugates, thus showing evidence for TRPA1 activation by covalent lysine modification.
[Mh] Termos MeSH primário: Canais de Cálcio/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Extratos Vegetais/química
Sesquiterpenos/química
Paladar
Canais de Receptores Transientes de Potencial/metabolismo
Winteraceae/química
[Mh] Termos MeSH secundário: Adulto
Animais
Células CHO
Cálcio/metabolismo
Canais de Cálcio/genética
Cricetulus
Feminino
Seres Humanos
Masculino
Camundongos
Camundongos Knockout
Proteínas do Tecido Nervoso/genética
Extratos Vegetais/metabolismo
Sesquiterpenos/metabolismo
Canal de Cátion TRPA1
Canais de Receptores Transientes de Potencial/genética
Winteraceae/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channels); 0 (Nerve Tissue Proteins); 0 (Plant Extracts); 0 (Sesquiterpenes); 0 (TRPA1 Cation Channel); 0 (TRPA1 protein, human); 0 (Transient Receptor Potential Channels); 0 (Trpa1 protein, mouse); 0 (drimane); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170629
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b02356


  7 / 925 MEDLINE  
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[PMID]:28648659
[Au] Autor:Bellono NW; Bayrer JR; Leitch DB; Castro J; Zhang C; O'Donnell TA; Brierley SM; Ingraham HA; Julius D
[Ad] Endereço:Department of Physiology, University of California, San Francisco, San Francisco, CA 94143, USA.
[Ti] Título:Enterochromaffin Cells Are Gut Chemosensors that Couple to Sensory Neural Pathways.
[So] Source:Cell;170(1):185-198.e16, 2017 Jun 29.
[Is] ISSN:1097-4172
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dietary, microbial, and inflammatory factors modulate the gut-brain axis and influence physiological processes ranging from metabolism to cognition. The gut epithelium is a principal site for detecting such agents, but precisely how it communicates with neural elements is poorly understood. Serotonergic enterochromaffin (EC) cells are proposed to fulfill this role by acting as chemosensors, but understanding how these rare and unique cell types transduce chemosensory information to the nervous system has been hampered by their paucity and inaccessibility to single-cell measurements. Here, we circumvent this limitation by exploiting cultured intestinal organoids together with single-cell measurements to elucidate intrinsic biophysical, pharmacological, and genetic properties of EC cells. We show that EC cells express specific chemosensory receptors, are electrically excitable, and modulate serotonin-sensitive primary afferent nerve fibers via synaptic connections, enabling them to detect and transduce environmental, metabolic, and homeostatic information from the gut directly to the nervous system.
[Mh] Termos MeSH primário: Células Quimiorreceptoras/metabolismo
Células Enterocromafins/metabolismo
Trato Gastrointestinal/citologia
Vias Neurais
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Sequência de Bases
Canais de Cálcio/metabolismo
Catecolaminas/metabolismo
Perfilação da Expressão Gênica
Seres Humanos
Síndrome do Intestino Irritável/patologia
Camundongos
Fibras Nervosas/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Receptores Odorantes/metabolismo
Receptores 5-HT3 de Serotonina/metabolismo
Serotonina/metabolismo
Transdução de Sinais
Sinapses/metabolismo
Canal de Cátion TRPA1
Canais de Receptores Transientes de Potencial/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channels); 0 (Catecholamines); 0 (Nerve Tissue Proteins); 0 (Olfr558 protein, mouse); 0 (Receptors, Odorant); 0 (Receptors, Serotonin, 5-HT3); 0 (TRPA1 Cation Channel); 0 (TRPA1 protein, human); 0 (Transient Receptor Potential Channels); 333DO1RDJY (Serotonin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170627
[St] Status:MEDLINE


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[PMID]:28644897
[Au] Autor:Sinharoy P; Bratz IN; Sinha S; Showalter LE; Andrei SR; Damron DS
[Ad] Endereço:Department of Anesthesia, Perioperative and Pain Medicine, Stanford School of Medicine, Stanford, California, United States of America.
[Ti] Título:TRPA1 and TRPV1 contribute to propofol-mediated antagonism of U46619-induced constriction in murine coronary arteries.
[So] Source:PLoS One;12(6):e0180106, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Transient receptor potential (TRP) ion channels have emerged as key components contributing to vasoreactivity. Propofol, an anesthetic is associated with adverse side effects including hypotension and acute pain upon infusion. Our objective was to determine the extent to which TRPA1 and/or TRPV1 ion channels are involved in mediating propofol-induced vasorelaxation of mouse coronary arterioles in vitro and elucidate the potential cellular signal transduction pathway by which this occurs. METHODS: Hearts were excised from anesthetized mice and coronary arterioles were dissected from control C57Bl/6J, TRPA1-/-, TRPV1-/- and double-knockout mice (TRPAV-/-). Isolated microvessels were cannulated and secured in a temperature-controlled chamber and allowed to equilibrate for 1 hr. Vasoreactivity studies were performed in microvessels pre-constricted with U46619 to assess the dose-dependent relaxation effects of propofol on coronary microvascular tone. RESULTS: Propofol-induced relaxation was unaffected in vessels obtained from TRPV1-/- mice, markedly attenuated in pre-constricted vessels obtained from TRPA1-/- mice and abolished in vessels obtained from TRPAV-/- mice. Furthermore, NOS inhibition with L-NAME or endothelium denuding abolished the proporfol-induced depressor response in pre-constricted vessels obtained from all mice. In the absence of L-NAME, BKCa inhibition with penitrem A markedly attenuated propofol-mediated relaxation in vessels obtained from wild-type mice and to a lesser extent in vessels obtained from TRPV1-/-, mice with no effect in vessels obtained from TRPA1-/- or TRPAV-/- mice. CONCLUSIONS: TRPA1 and TRPV1 appear to contribute to the propofol-mediated antagonism of U46619-induced constriction in murine coronary microvessels that involves activation of NOS and BKCa.
[Mh] Termos MeSH primário: Ácido 15-Hidroxi-11 alfa,9 alfa-(epoximetano)prosta-5,13-dienoico/antagonistas & inibidores
Vasos Coronários/efeitos dos fármacos
Propofol/farmacologia
Canais de Cátion TRPV/metabolismo
Canais de Receptores Transientes de Potencial/metabolismo
Vasodilatadores/farmacologia
[Mh] Termos MeSH secundário: Ácido 15-Hidroxi-11 alfa,9 alfa-(epoximetano)prosta-5,13-dienoico/farmacologia
Animais
Células Cultivadas
Vasos Coronários/metabolismo
Células Endoteliais/efeitos dos fármacos
Células Endoteliais/metabolismo
Subunidades alfa do Canal de Potássio Ativado por Cálcio de Condutância Alta/metabolismo
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Microvasos/efeitos dos fármacos
Microvasos/metabolismo
Óxido Nítrico Sintase Tipo III/metabolismo
Canal de Cátion TRPA1
Canais de Cátion TRPV/genética
Canais de Receptores Transientes de Potencial/genética
Vasoconstritores/antagonistas & inibidores
Vasoconstritores/farmacologia
Vasodilatação/efeitos dos fármacos
Vasodilatação/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BKCa protein, mouse); 0 (Large-Conductance Calcium-Activated Potassium Channel alpha Subunits); 0 (TRPA1 Cation Channel); 0 (TRPV Cation Channels); 0 (TRPV1 protein, mouse); 0 (Transient Receptor Potential Channels); 0 (Trpa1 protein, mouse); 0 (Vasoconstrictor Agents); 0 (Vasodilator Agents); 76898-47-0 (15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid); EC 1.14.13.39 (Nitric Oxide Synthase Type III); EC 1.14.13.39 (Nos3 protein, mouse); YI7VU623SF (Propofol)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170624
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180106


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[PMID]:28640016
[Au] Autor:Sugiyama D; Kang S; Arpey N; Arunakul P; Usachev YM; Brennan TJ
[Ad] Endereço:From the Departments of Anesthesia (D.S., S.K., N.A., P.A., T.J.B.) and Pharmacology (Y.M.U., T.J.B.), Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, Iowa.
[Ti] Título:Hydrogen Peroxide Induces Muscle Nociception via Transient Receptor Potential Ankyrin 1 Receptors.
[So] Source:Anesthesiology;127(4):695-708, 2017 Oct.
[Is] ISSN:1528-1175
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: H2O2 has a variety of actions in skin wounds but has been rarely studied in deep muscle tissue. Based on response to the transient receptor potential ankyrin 1 antagonists after plantar incision, we hypothesized that H2O2 exerts nociceptive effects via the transient receptor potential ankyrin 1 in muscle. METHODS: Nociceptive behaviors in rats (n = 269) and mice (n = 16) were evaluated after various concentrations and volumes of H2O2 were injected into the gastrocnemius muscle or subcutaneous tissue. The effects of H2O2 on in vivo spinal dorsal horn neuronal activity and lumbar dorsal root ganglia neurons in vitro were evaluated from 26 rats and 6 mice. RESULTS: Intramuscular (mean ± SD: 1,436 ± 513 s) but not subcutaneous (40 ± 58 s) injection of H2O2 (100 mM, 0.6 ml) increased nociceptive time. Conditioned place aversion was evident after intramuscular (-143 ± 81 s) but not subcutaneous (-2 ± 111 s) injection of H2O2. These H2O2-induced behaviors were blocked by transient receptor potential ankyrin 1 antagonists. Intramuscular injection of H2O2 caused sustained in vivo activity of dorsal horn neurons, and H2O2 activated a subset of dorsal root ganglia neurons in vitro. Capsaicin nerve block decreased guarding after plantar incision and reduced nociceptive time after intramuscular H2O2. Nociceptive time after intramuscular H2O2 in transient receptor potential ankyrin 1 knockout mice was shorter (173 ± 156 s) compared with wild-type mice (931 ± 629 s). CONCLUSIONS: The greater response of muscle tissue to H2O2 may help explain why incision that includes deep muscle but not skin incision alone produces spontaneous activity in nociceptive pathways.
[Mh] Termos MeSH primário: Peróxido de Hidrogênio/farmacologia
Músculo Esquelético/efeitos dos fármacos
Nociceptividade/efeitos dos fármacos
Canais de Cátion TRPC/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Anti-Infecciosos Locais/farmacologia
Modelos Animais de Doenças
Feminino
Gânglios Espinais/efeitos dos fármacos
Masculino
Nociceptores/efeitos dos fármacos
Células do Corno Posterior/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
Canal de Cátion TRPA1
Canais de Cátion TRPC/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Infective Agents, Local); 0 (TRPA1 Cation Channel); 0 (TRPC Cation Channels); 0 (Trpa1 protein, rat); BBX060AN9V (Hydrogen Peroxide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.1097/ALN.0000000000001756


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[PMID]:28629997
[Au] Autor:Takahashi K; Ohta T
[Ad] Endereço:Department of Veterinary Pharmacology, Faculty of Agriculture, Tottori University, 680-8553, Japan. Electronic address: takahashi@muses.tottori-u.ac.jp.
[Ti] Título:Membrane translocation of transient receptor potential ankyrin 1 induced by inflammatory cytokines in lung cancer cells.
[So] Source:Biochem Biophys Res Commun;490(3):587-593, 2017 Aug 26.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Transient receptor potential ankyrin 1 (TRPA1) is known as one of the nociceptors expressed in sensory neurons. It also plays a role in non-neural cells in inflammatory sites. However, the regulatory mechanisms for the reactivity of TRPA1 in these cells under inflammatory conditions are not clear. To clarify these mechanisms, we examined the effects of inflammatory cytokines (interleukin [IL]-1α, IL-1ß and tumor necrosis factor α [TNFα]) on TRPA1 reactivity and expression in the endogenously TRPA1-expressing lung tumor cell line A549. Treatment with IL-1α, but not IL-1ß or TNFα, increased the number of cells responding to allyl isothiocyanate, a TRPA1 agonist, in a dose- and time-dependent manner. The IL-1α-induced increase of TRPA1 responsiveness was inhibited by an extracellular-regulated kinase (Erk) inhibitor (PD98059) but not by inhibitors of c-Jun kinase, p38 mitogen-activated protein kinase or phosphatidylinositol-3 kinase. Phosphorylation of Erk gradually increased at 24 h after its transient induction in cells treated with IL-1α. IL-1α increased the TRPA1 levels on biotinylated cell surface proteins. These results suggest that IL-1α enhances the translocation of TRPA1 to the plasma membrane via the activation of Erk in A549. TRPA1 may have a pathophysiological role in non-neural lung cells under inflammatory conditions.
[Mh] Termos MeSH primário: Canais de Cálcio/imunologia
Interleucina-1alfa/imunologia
Neoplasias Pulmonares/imunologia
Pulmão/imunologia
Proteínas do Tecido Nervoso/imunologia
Canais de Receptores Transientes de Potencial/imunologia
[Mh] Termos MeSH secundário: Células A549
Membrana Celular/imunologia
Membrana Celular/metabolismo
Seres Humanos
Inflamação/imunologia
Inflamação/metabolismo
Interleucina-1alfa/análise
Interleucina-1alfa/metabolismo
Interleucina-1beta/imunologia
Pulmão/metabolismo
Neoplasias Pulmonares/metabolismo
Proteína Quinase 1 Ativada por Mitógeno/imunologia
Proteína Quinase 3 Ativada por Mitógeno/imunologia
Transporte Proteico
Canal de Cátion TRPA1
Fator de Necrose Tumoral alfa/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channels); 0 (IL1A protein, human); 0 (Interleukin-1alpha); 0 (Interleukin-1beta); 0 (Nerve Tissue Proteins); 0 (TRPA1 Cation Channel); 0 (TRPA1 protein, human); 0 (Transient Receptor Potential Channels); 0 (Tumor Necrosis Factor-alpha); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170621
[St] Status:MEDLINE



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