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Glia and Glia-Neuron Interaction

開催日 2014/9/13
時間 11:00 - 12:00
会場 Poster / Exhibition(Event Hall B)

Involvement of nitric oxide in the induction of interleukin 1 β in microglia in vitro

  • P3-023
  • 中嶋 一行 / Kazuyuki Nakajima:1 瀧澤 光子 / Mitsuko Takizawa:1 小林 裕志 / Hiroshi Kobayashi:1 高坂 新一 / Shinichi Kohsaka:2 
  • 1:創価大学 / Dept. of Bioinformatics, Faculty of Engineering, Soka Univ. 2:国立精神・神経医療研究センター 神経研究所 / National Institute of Neuroscience, Tokyo, Japan 

Microglia in vitro induced an inflammatory cytokine interleukin 1β (IL-1β) together with nitric oxide (NO) and superoxide anion (O2-) by stimulation with lipopolysaccharide (LPS). In this study, we investigated the role of NO and O2- in the signaling mechanism by which IL-1β is induced in LPS-stimulated microglia. The LPS-inducible IL-1β was significantly suppressed by pretreatment with the NO scavenger 2-(4-carboxyphenyl)-4,4,5, 5-tetramethylimidazoline-1-oxyl 3-oxide, but not by O2- scavenger N-acetyl cystein, suggesting the close association of NO with IL-1β induction. The pretreatment of microglia with iNOS inhibitor 1400w prior to LPS stimulation significantly reduced the production of IL-1β. On the other hand, the addition of NO-donor S-nitroso-N-acetyl-DL-penicillamine (SNAP) into microglia led to the induction of IL-1β. In this SNAP stimulation, extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) were activated in microglia, suggesting the necessity of ERK/JNK activation in IL-1β induction. In fact, LPS-inducible IL-1β production was significantly suppressed by pretreatment with ERK inhibitor or JNK inhibitor. Taken together, these results indicated that NO is an important signaling molecule for activating ERK/JNK, which are requisite for inducing IL-1β in microglia.

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