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Satellite glial cells express IL-6 and corresponding signal-transducing receptors in the dorsal root ganglia of rat neuropathic pain model
P. Dubový, I. Klusáková, I. Svízenská, V. Brázda,
Jazyk angličtina Země Anglie, Velká Británie
Typ dokumentu časopisecké články, práce podpořená grantem
NLK
ProQuest Central
od 2004-02-01 do 2011-11-30
Health & Medicine (ProQuest)
od 2004-02-01 do 2011-11-30
Psychology Database (ProQuest)
od 2004-02-01 do 2011-11-30
- MeSH
- cytokinový receptor gp130 genetika metabolismus MeSH
- funkční lateralita MeSH
- interleukin-6 genetika metabolismus MeSH
- krysa rodu rattus MeSH
- měření bolesti MeSH
- messenger RNA metabolismus MeSH
- modely nemocí na zvířatech MeSH
- nemoci sedacího nervu patologie patofyziologie MeSH
- neuroglie metabolismus MeSH
- potkani Wistar MeSH
- receptory interleukinu-6 genetika metabolismus MeSH
- regulace genové exprese fyziologie MeSH
- signální transdukce fyziologie MeSH
- spinální ganglia patologie patofyziologie MeSH
- transkripční faktor STAT3 metabolismus MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
There is a growing body of evidence that cytokines contribute to both induction and maintenance of neuropathic pain derived from changes in dorsal root ganglia (DRG), including the activity of the primary sensory neurons and their satellite glial cells (SGC). We used immunofluorescence and in situ hybridization methods to provide evidence that chronic constriction injury (CCI) of the sciatic nerve induces synthesis of interleukin-6 (IL-6) in SGC, elevation of IL-6 receptor (IL-6R) and activation of signal transducer and activator of transcription 3 (STAT3) signalling. Unilateral CCI of the rat sciatic nerve induced mechanoallodynia and thermal hyperalgesia in ipsilateral hind paws, but contralateral paws exhibited only temporal changes of sensitivity. We demonstrated that IL-6 mRNA and protein, which were expressed at very low levels in naïve DRG, were bilaterally increased not only in L4-L5 DRG neurons but also in SGC activated by unilateral CCI. Besides IL-6, substantial increase of IL-6R and pSTAT3 expression occurred in SGC following CCI, however, IL-6R associated protein, gp130 levels did not change. The results may suggest that unilateral CCI of the sciatic nerve induces bilateral activation of SGC in L4-L5 DRG to transduce IL-6 signalling during neuroinflammation.
Citace poskytuje Crossref.org
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