Document Detail

Differential nuclear factor-kappa B phosphorylation induced by lipopolysaccharide in the hippocampus of P2X7 receptor knockout mouse.
MedLine Citation:
PMID:  23540405     Owner:  NLM     Status:  In-Data-Review    
OBJECTIVE: Lipopolysaccharide (LPS) stimulates the innate immune response in the brain through nuclear factor-kappaB (NF-kappaB) signaling. Since purinergic signals activate NF-kappaB through the P2X7 receptor (P2X7R), we investigated the roles of P2X7R in neuronal NF-kappaB phosphorylation in the mouse hippocampus under basal conditions and P2X7R deletion following LPS treatment in vivo.
METHODS: We performed immunohistochemical studies for neuronal NF-kappaB phosphorylation in the hippocampi of wild type (WT) and P2X7R knockout (KO) mice under basal conditions and LPS treatment.
RESULTS: LPS treatment did not induce neuronal damages in both WT and P2X7(-/-) KO mice. In WT animals, LPS treatment increased p65-Ser276 and p65-Ser311 NF-kappaB phosphorylations in hippocampal neurons. However, p52-Ser865, p52-Ser869, p65-Ser468, p65-Ser529, and p65-Ser536 NF-kappaB phosphorylations were unaffected by LPS treatment. In P2X7(-/-) KO mice, neuronal p65-Ser311 NF-kappaB phosphorylation in vehicle-treated animals was higher than that in WT animals. In addition, both p65-Ser276 and p65-Ser311 NF-kappaB phosphorylations were unaffected by LPS treatment in P2X7(-/-) KO mice.
DISCUSSION: These findings indicate that P2X7R may be involved in LPS-induced inflammatory response in neurons, and that p65-Ser311 NF-kappaB phosphorylation may compensate for the loss function of P2X7R by as yet unknown factors.
Won Il Kim; Hea Jin Ryu; Ji-Eun Kim; Cheong Hoon Seo; Boung Chul Lee; Ihn-Geun Choi; Tae-Cheon Kang
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Neurological research     Volume:  35     ISSN:  1743-1328     ISO Abbreviation:  Neurol. Res.     Publication Date:  2013 May 
Date Detail:
Created Date:  2013-04-01     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7905298     Medline TA:  Neurol Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  369-81     Citation Subset:  IM    
Hallym University, Kangwon-Do, Korea.
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