Satellite glial cells express IL-6 and corresponding signal-transducing receptors in the dorsal root ganglia of rat neuropathic pain model
Language English Country Great Britain, England Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
20519054
DOI
10.1017/s1740925x10000074
PII: S1740925X10000074
Knihovny.cz E-resources
- MeSH
- Cytokine Receptor gp130 genetics metabolism MeSH
- Functional Laterality MeSH
- Interleukin-6 genetics metabolism MeSH
- Rats MeSH
- Pain Measurement MeSH
- RNA, Messenger metabolism MeSH
- Disease Models, Animal MeSH
- Sciatic Neuropathy pathology physiopathology MeSH
- Neuroglia metabolism MeSH
- Rats, Wistar MeSH
- Receptors, Interleukin-6 genetics metabolism MeSH
- Gene Expression Regulation physiology MeSH
- Signal Transduction physiology MeSH
- Ganglia, Spinal pathology physiopathology MeSH
- STAT3 Transcription Factor metabolism MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Cytokine Receptor gp130 MeSH
- Interleukin-6 MeSH
- RNA, Messenger MeSH
- Receptors, Interleukin-6 MeSH
- STAT3 Transcription Factor 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.
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