Article

Increased phosphorylation of cyclic AMP response element-binding protein in the spinal cord of Lewis rats with experimental autoimmune encephalomyelitis.

Department of Veterinary Medicine and Applied Radiological Science Research Institute, Cheju National University, Jeju 690-756, South Korea.
Brain Research (impact factor: 2.73). 09/2007; 1162:113-20. DOI:10.1016/j.brainres.2007.05.072 pp.113-20
Source: PubMed

ABSTRACT To investigate whether the phosphorylation of cyclic AMP response element-binding protein (CREB) is implicated in the pathogenesis of experimental autoimmune encephalomyelitis (EAE), the change in the level of CREB phosphorylation was analyzed in the spinal cord of Lewis rats with EAE. Western blot analysis showed that the phosphorylation of CREB in the spinal cord of rats increased significantly at the peak stage of EAE compared with the controls (p<0.05) and declined significantly in the recovery stage (p<0.05). Immunohistochemistry showed that the phosphorylated form of CREB (p-CREB) was constitutively immunostained in few astrocytes and dorsal horn neurons in the spinal cord of normal rats. In the EAE-affected spinal cord, p-CREB was mainly found in ED1-positive macrophages at the peak stage of EAE, and the number of p-CREB-immunopositive astrocytes was markedly increased in the spinal cord with EAE compared with the controls. Moreover, p-CREB immunoreactivity of sensory neurons, which are closely associated with neuropathic pain, was significantly increased in the dorsal horns at the peak stage of EAE. Based on these results, we suggest that the increased phosphorylation of CREB in EAE lesions was mainly attributable to the infiltration of inflammatory cells and astrogliosis, possibly activating gene transcription, and that its increase in the sensory neurons in the dorsal horns is involved in the generation of neuropathic pain in the rat EAE model.

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    Article: The role of kinin receptors in preventing neuroinflammation and its clinical severity during experimental autoimmune encephalomyelitis in mice.
    Rafael C Dutra, Daniela F P Leite, Allisson F Bento, Marianne N Manjavachi, Eliziane S Patrício, Cláudia P Figueiredo, João B Pesquero, João B Calixto
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    PLoS ONE 01/2011; 6(11):e27875. · 4.09 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.

Keywords

activating gene transcription
 
cyclic AMP response element-binding protein
 
dorsal horn neurons
 
dorsal horns
 
EAE lesions
 
EAE-affected spinal cord
 
ED1-positive macrophages
 
experimental autoimmune encephalomyelitis
 
inflammatory cells
 
Lewis rats
 
neuropathic pain
 
p-CREB immunoreactivity
 
p-CREB-immunopositive astrocytes
 
p<0.05). Immunohistochemistry
 
pathogenesis
 
peak stage
 
phosphorylated form
 
rat EAE model
 
recovery stage
 
spinal cord