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演題詳細

Poster

神経保護、神経毒性と神経炎症
Neuroprotection, Neurotoxicity and Neuroinflammation

開催日 2014/9/11
時間 16:00 - 17:00
会場 Poster / Exhibition(Event Hall B)

低酸素状態におけるNO誘導性シュワン細胞株の死
Nitric oxide induced Schannoma cell death in hypoxia

  • P1-338
  • 中村 俊一郎 / Shunichiro Nakamura:1 井上 宏子 / hiroko inoue:1 
  • 1:早稲田大学大学院 / Waseda University, Tokyo, Japan 

Nitric oxide induced Schwann cell death in hypoxia.
Shunichiro Nakamura, Waseda University

Reactive nitrogen species (nitric oxide (NO) and peroxynitrite (ONOO-)) have been shown to initiate apoptotic cell death. ONOO-, which is a potent oxidant, is generated by reaction between NO and the superoxide anion (O2-). The mechanism of NO-induced cell death is well investigated in several cells, but not in Schwann cells. The partial pressure of oxygen (pO2) in the brain is 30-45 mmHg (approximately 4% O2) and proliferation is enhanced under physiological O2 conditions. Therefore, in this study, we examined NO-induced cell death during hypoxia (i.e., 4% O2) in RT4-D6P2T Schwann cells. The cells were treated with 300-550 μM sodium nitroprusside (SNP) for 24 hours under both hypoxic and normoxic conditions, and cell viability was measured using the crystal violet assay. The half maximal inhibitory concentration (IC50) was 450 and 350 μM during hypoxia and normoxia, respectively. Mitogen-activated protein kinases (MAPKs) have been reported to be activated during hypoxia. Thus, we investigated whether MAPKs were related to SNP-induced cell death. For drug pretreatment, RT4-D6P2T cells were incubated with SB203580 (p38 inhibiter), SP600125 (JNK inhibiter), or PD98059 (ERK1/2) for 1 hour before the addition of SNP. SB203580 increased cell viability under the hypoxic condition, but not under the normoxic condition. On the other hand, SP600125 and PD98059 did not affect cell viability. When the protein expression of p38 was analyzed by Western blotting, phosphorylated p38 increased during hypoxia, but not during normoxia. Therefore, our results suggest that the p38 signal pathway may play a crucial role in cell death induced by SNP under the hypoxic condition.

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