Resolvin E1 Inhibits Substance P-Induced Potentiation of TRPV1 in Primary Sensory Neurons
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Jo, Youn Yi | - |
dc.contributor.author | Lee, Ji Yeon | - |
dc.contributor.author | Park, Chul-Kyu | - |
dc.date.available | 2020-02-28T06:44:44Z | - |
dc.date.created | 2020-02-06 | - |
dc.date.issued | 2016 | - |
dc.identifier.issn | 0962-9351 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/9785 | - |
dc.description.abstract | The neuropeptide substance P (SP) is expressed in primary sensory neurons and is commonly regarded as a "pain" neurotransmitter. Upon peripheral inflammation, SP activates the neurokinin-1 (NK-1) receptor and potentiates activity of transient receptor potential vanilloid subtype 1 (TRPV1), which is coexpressed by nociceptive neurons. Therefore, SP functions as an important neurotransmitter involved in the hypersensitization of inflammatory pain. Resolvin E1 (RvE1), derived from omega-3 polyunsaturated fatty acids, inhibits TRPV1 activity via activation of the chemerin 23 receptor (ChemR23)-an RvE1 receptor located in dorsal root ganglion neurons-and therefore exerts an inhibitory effect on inflammatory pain. We demonstrate here that RvE1 regulates the SP-induced potentiation of TRPV1 via G-protein coupled receptor (GPCR) on peripheral nociceptive neurons. SP-induced potentiation of TRPV1 inhibited by RvE1 was blocked by the G alpha i-coupled GPCR inhibitor pertussis toxin and the G-protein inhibitor GDP beta-S. These results indicate that a low concentration of RvE1 strongly inhibits the potentiation of TRPV1, induced by the SP-mediated activation of NK-1, via a GPCR signaling pathway activated by ChemR23 in nociceptive neurons. RvE1 might represent a new therapeutic target for the treatment of inflammatory pain as a prospective endogenous inhibitor that strongly inhibits TRPV1 activity associated with peripheral inflammation. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | HINDAWI LTD | - |
dc.relation.isPartOf | MEDIATORS OF INFLAMMATION | - |
dc.subject | CORD SYNAPTIC PLASTICITY | - |
dc.subject | PRIMARY AFFERENT NEURONS | - |
dc.subject | ROOT GANGLION NEURONS | - |
dc.subject | INFLAMMATORY PAIN | - |
dc.subject | NK1 RECEPTOR | - |
dc.subject | NEUROKININ-1 RECEPTORS | - |
dc.subject | TACHYKININ RECEPTOR | - |
dc.subject | CAPSAICIN RECEPTOR | - |
dc.subject | HEAT HYPERALGESIA | - |
dc.subject | LIPID MEDIATORS | - |
dc.title | Resolvin E1 Inhibits Substance P-Induced Potentiation of TRPV1 in Primary Sensory Neurons | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000385194300001 | - |
dc.identifier.doi | 10.1155/2016/5259321 | - |
dc.identifier.bibliographicCitation | MEDIATORS OF INFLAMMATION | - |
dc.identifier.scopusid | 2-s2.0-84991383465 | - |
dc.citation.title | MEDIATORS OF INFLAMMATION | - |
dc.contributor.affiliatedAuthor | Jo, Youn Yi | - |
dc.contributor.affiliatedAuthor | Lee, Ji Yeon | - |
dc.contributor.affiliatedAuthor | Park, Chul-Kyu | - |
dc.type.docType | Article | - |
dc.subject.keywordPlus | CORD SYNAPTIC PLASTICITY | - |
dc.subject.keywordPlus | PRIMARY AFFERENT NEURONS | - |
dc.subject.keywordPlus | ROOT GANGLION NEURONS | - |
dc.subject.keywordPlus | INFLAMMATORY PAIN | - |
dc.subject.keywordPlus | NK1 RECEPTOR | - |
dc.subject.keywordPlus | NEUROKININ-1 RECEPTORS | - |
dc.subject.keywordPlus | TACHYKININ RECEPTOR | - |
dc.subject.keywordPlus | CAPSAICIN RECEPTOR | - |
dc.subject.keywordPlus | HEAT HYPERALGESIA | - |
dc.subject.keywordPlus | LIPID MEDIATORS | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalResearchArea | Immunology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Immunology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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