1: Neuroscience. 2005;133(3):797-806. 

Up-regulated phosphorylation of signal transducer and activator of transcription
3 and cyclic AMP-responsive element binding protein by peripheral inflammation
in primary afferent neurons possibly through oncostatin M receptor.

Tamura S, Morikawa Y, Senba E.

Department of Anatomy and Neurobiology, Wakayama Medical University, Kimiidera
811-1, Wakayama 641-8509, Japan.

Oncostatin M (OSM), a member of interleukin-6 family cytokines, contributes to
the development of nociceptive sensory neurons. However, little is known about
the role of OSM in dorsal root ganglia (DRGs) of adult mice after peripheral
inflammation. In the present study, we showed that OSM mRNA was highly expressed
in the inflamed skin during acute inflammation induced by complete Freund's
adjuvant (CFA), while the expression of oncostatin M receptor (OSMR) did not
change in the ipsilateral DRG. Although peripheral inflammation induced
significant increases in the number of neurons with phosphorylated extracellular
signal-regulated kinase (p-ERK) and phosphorylated p38 mitogen-activated protein
kinase (p-p38) in ipsilateral DRGs, OSMR-positive neurons exhibited neither
p-ERK nor p-p38. In addition, we found significant increases in the number of
neurons with phosphorylated signal transducer and activator of transcription 3
(p-STAT3) and phosphorylated cAMP-responsive element binding protein (p-CREB) in
the ipsilateral DRGs. Interestingly, OSMR-positive neurons with p-STAT3 and
p-CREB were significantly increased after peripheral inflammation. Thus, our
results suggest that acute inflammation induce the phosphorylations of several
signal molecules, including ERK, p38, cAMP-responsive element binding protein,
and STAT3. Among them, the up-regulation of p-STAT3 and p-CREB may be induced
possibly through OSMR.

PMID: 15893881 [PubMed - indexed for MEDLINE]


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