pubmed-article:17470568 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17470568 | lifeskim:mentions | umls-concept:C0151744 | lld:lifeskim |
pubmed-article:17470568 | lifeskim:mentions | umls-concept:C0521390 | lld:lifeskim |
pubmed-article:17470568 | lifeskim:mentions | umls-concept:C0013725 | lld:lifeskim |
pubmed-article:17470568 | lifeskim:mentions | umls-concept:C0035126 | lld:lifeskim |
pubmed-article:17470568 | lifeskim:mentions | umls-concept:C1421467 | lld:lifeskim |
pubmed-article:17470568 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
pubmed-article:17470568 | pubmed:issue | 11 | lld:pubmed |
pubmed-article:17470568 | pubmed:dateCreated | 2007-9-3 | lld:pubmed |
pubmed-article:17470568 | pubmed:abstractText | Recent evidence implicates the neuronal transient receptor potential vanilloid receptor 1 (TRPV1), expressed on sensory C-fibers, as playing an important endogenous protective role in limiting the damaging effects of myocardial I/R injury. In neurons the 12-lipoxygenase (12-LOX) arachidonic acid (AA) metabolite, 12(S)-HpETE, has been proposed as the endogenous ligand for TRPV1. However, whether 12(S)-HpETE underlies TRPV1 channel activation during I/R is unknown. Treatment of isolated Langendorff rat hearts with a 12-LOX/AA cocktail significantly attenuated I/R injury (approximately 40% inhibition of infarct size), an effect reversed by the 12-LOX inhibitor baicalein or after chemical desensitization of local sensory C-fiber afferents using capsaicin. Both 12(S)-HpETE and AA caused dose-dependent coronary vasodilatation (approximately EC50s of 6x10(-19) and 1x10(-7), respectively) that was profoundly suppressed by the TRPV1 antagonist capsazepine, in hearts of TRPV1 knockout mice compared with wild-type mice, or by treatment with a CGRP antagonist. In addition, I/R itself stimulates up-regulation of TRPV1 expression in both the cell bodies located within the dorsal root ganglia and locally within the myocardium. Together, our data identify a novel 12-LOX/AA/TRPV1 pathway activated and up-regulated during I/R injury, providing an endogenous damage-limiting mechanism whose targeting may prove useful in treating myocardial infarction. | lld:pubmed |
pubmed-article:17470568 | pubmed:language | eng | lld:pubmed |
pubmed-article:17470568 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17470568 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:17470568 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:17470568 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:17470568 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17470568 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17470568 | pubmed:month | Sep | lld:pubmed |
pubmed-article:17470568 | pubmed:issn | 1530-6860 | lld:pubmed |
pubmed-article:17470568 | pubmed:author | pubmed-author:CaylaCecileC | lld:pubmed |
pubmed-article:17470568 | pubmed:author | pubmed-author:AhluwaliaAmri... | lld:pubmed |
pubmed-article:17470568 | pubmed:author | pubmed-author:McDonaldMiche... | lld:pubmed |
pubmed-article:17470568 | pubmed:author | pubmed-author:SextonAlisonA | lld:pubmed |
pubmed-article:17470568 | pubmed:author | pubmed-author:ThiemermannCh... | lld:pubmed |
pubmed-article:17470568 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:17470568 | pubmed:volume | 21 | lld:pubmed |
pubmed-article:17470568 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17470568 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17470568 | pubmed:pagination | 2695-703 | lld:pubmed |
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pubmed-article:17470568 | pubmed:year | 2007 | lld:pubmed |
pubmed-article:17470568 | pubmed:articleTitle | 12-Lipoxygenase-derived eicosanoids protect against myocardial ischemia/reperfusion injury via activation of neuronal TRPV1. | lld:pubmed |
pubmed-article:17470568 | pubmed:affiliation | William Harvey Research Institute, Barts and The London Medical School, Queen Mary University of London, Charterhouse Square, London, UK. | lld:pubmed |
pubmed-article:17470568 | pubmed:publicationType | Journal Article | lld:pubmed |
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