Linked Life Data

19683949

Source:http://linkedlifedata.com/resource/pubmed/id/19683949

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2010-4-2
pubmed:abstractText
Protease-activated receptor-2 (PAR-2) is a G-protein-coupled receptor activated through proteolytic cleavage. It is localized on epithelial, endothelial and inflammatory cells, as well as on transient receptor potential vanilloid 1 (TRPV1) receptor-expressing neurones. It plays an important role in inflammatory/nociceptive processes. Since there are few reports concerning PAR-2 function in joints, the effects of intraarticular PAR-2 activation on joint pain and inflammation were studied. Secondary hyperalgesia/allodynia, spontaneous weight distribution, swelling and inflammatory cytokine production were measured and the involvement of TRPV1 ion channels was investigated in rats and mice. Injection of the PAR-2 receptor agonist SLIGRL-NH(2) into the knee decreased touch sensitivity and weight bearing of the ipsilateral hindlimb in both species. Secondary mechanical allodynia/hyperalgesia and impaired weight distribution were significantly reduced by the TRPV1 antagonist SB366791 in rats and by the genetic deletion of this receptor in mice. PAR-2 activation did not cause significant joint swelling, but increased IL-1beta concentration which was not influenced by the lack of the TRPV1 channel. For comparison, intraplantar SLIGRL-NH(2) evoked similar primary mechanical hyperalgesia and impaired weight distribution in both WT and TRPV1 deficient mice, but oedema was smaller in the knockouts. The inactive peptide, LRGILS-NH(2), injected into either site did not induce any inflammatory or nociceptive changes. These data provide evidence for a significant role of TRPV1 receptors in secondary mechanical hyperalgesia/allodynia and spontaneous pain induced by PAR-2 receptor activation in the knee joint. Although intraplantar PAR-2 activation-induced oedema is also TRPV1 receptor-mediated, primary mechanical hyperalgesia, impaired weight distribution and IL-1beta production are independent of this channel.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1532-2149
pubmed:author
pubmed:copyrightInfo
Copyright (c) 2009 European Federation of International Association for the Study of Pain Chapters. Published by Elsevier Ltd. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
351-8
pubmed:meshHeading
pubmed-meshheading:19683949-Anilides, pubmed-meshheading:19683949-Animals, pubmed-meshheading:19683949-Arthritis, pubmed-meshheading:19683949-Body Weight, pubmed-meshheading:19683949-Cinnamates, pubmed-meshheading:19683949-Cytokines, pubmed-meshheading:19683949-Enzyme Activation, pubmed-meshheading:19683949-Foot, pubmed-meshheading:19683949-Hindlimb, pubmed-meshheading:19683949-Hyperalgesia, pubmed-meshheading:19683949-Injections, Intra-Articular, pubmed-meshheading:19683949-Male, pubmed-meshheading:19683949-Mechanoreceptors, pubmed-meshheading:19683949-Mice, pubmed-meshheading:19683949-Mice, Inbred C57BL, pubmed-meshheading:19683949-Oligopeptides, pubmed-meshheading:19683949-Pain, pubmed-meshheading:19683949-Pain Measurement, pubmed-meshheading:19683949-Pain Threshold, pubmed-meshheading:19683949-Rats, pubmed-meshheading:19683949-Rats, Wistar, pubmed-meshheading:19683949-Receptor, PAR-2, pubmed-meshheading:19683949-TRPV Cation Channels
pubmed:year
2010
pubmed:articleTitle
Involvement of transient receptor potential vanilloid 1 receptors in protease-activated receptor-2-induced joint inflammation and nociception.
pubmed:affiliation
Department of Pharmacology and Pharmacotherapy, Faculty of Medicine, University of Pécs, H-7624 Pécs, Szigeti u. 12., Hungary. zsuzsanna.helyes@aok.pte.hu
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't