| http://purl.uniprot.org/citations/26166359 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/26166359 | http://www.w3.org/2000/01/rdf-schema#comment | "Immunity and neuroinflammation play major roles in neuropathic pain. Spinal interleukin (IL)-17A, as a mediator connecting innate and adaptive immunity, has been shown to be an important cytokine in neuroinflammation and acute neuropathic pain. However, the effects and underlying mechanisms of spinal IL-17A in the maintenance of neuropathic pain remain unknown. This study was designed to investigate whether spinal IL-17A acted to maintain neuropathic pain and to elucidate the underlying mechanisms in IL-17A knockout or wild-type (WT) mice following L4 spinal nerve ligation (L4 SNL). WT mice were treated with anti-IL-17A neutralized monoclonal antibody (mAb) or recombinant IL-17A (rIL-17A). We showed that IL-17A levels were significantly increased 1, 3, 7, and 14 days after SNL in spinal cord. Double immunofluorescence staining showed that astrocytes were the major cellular source of spinal IL-17A. IL-17A knockout or anti-IL-17A mAb treatment significantly ameliorated hyperalgesia 7 days after SNL, which was associated with a significant reduction of p-CaMKII and p-CREB levels in spinal cord, whereas rIL-17A treatment conferred the opposite effects. Furthermore, we showed that blocking CaMKII with KN93 significantly reduced SNL- or rIL-17A-induced hyperalgesia and p-CREB expression. Our in vitro data showed that KN93 also significantly inhibited rIL-17A-induced CREB activation in primary cultured spinal neurons. Taken together, our study indicates that astrocytic IL-17A plays important roles in the maintenance of neuropathic pain through CaMKII/CREB signaling pathway in spinal cord, and thus targeting IL-17A may offer an attractive strategy for the treatment of chronic persistent neuropathic pain."xsd:string |
| http://purl.uniprot.org/citations/26166359 | http://purl.org/dc/terms/identifier | "doi:10.1007/s12035-015-9322-z"xsd:string |
| http://purl.uniprot.org/citations/26166359 | http://purl.uniprot.org/core/author | "Feng T."xsd:string |
| http://purl.uniprot.org/citations/26166359 | http://purl.uniprot.org/core/author | "Lin Y."xsd:string |
| http://purl.uniprot.org/citations/26166359 | http://purl.uniprot.org/core/author | "Yao S."xsd:string |
| http://purl.uniprot.org/citations/26166359 | http://purl.uniprot.org/core/author | "Zhang J.C."xsd:string |
| http://purl.uniprot.org/citations/26166359 | http://purl.uniprot.org/core/author | "Yao C.Y."xsd:string |
| http://purl.uniprot.org/citations/26166359 | http://purl.uniprot.org/core/author | "Weng Z.L."xsd:string |
| http://purl.uniprot.org/citations/26166359 | http://purl.uniprot.org/core/date | "2016"xsd:gYear |
| http://purl.uniprot.org/citations/26166359 | http://purl.uniprot.org/core/name | "Mol Neurobiol"xsd:string |
| http://purl.uniprot.org/citations/26166359 | http://purl.uniprot.org/core/pages | "3914-3926"xsd:string |
| http://purl.uniprot.org/citations/26166359 | http://purl.uniprot.org/core/title | "Interleukin-17A Acts to Maintain Neuropathic Pain Through Activation of CaMKII/CREB Signaling in Spinal Neurons."xsd:string |
| http://purl.uniprot.org/citations/26166359 | http://purl.uniprot.org/core/volume | "53"xsd:string |
| http://purl.uniprot.org/citations/26166359 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/26166359 |
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