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Nerve growth factor-induced neuronal differentiation requires generation of Rac1-regulated reactive oxygen species

  1. Author:
    Suzukawa, K.
    Miura, K.
    Mitsushita, J.
    Resau, J.
    Hirose, K.
    Crystal, R.
    Kamata, T.

  2. Author Address

    Kamata T Shinshu Univ, Sch Med, Dept Mol Biol & Biochem Asahi 3-1-1 Nagano 3908621 Japan NCI, Sci Applicat Int Corp Frederick, Frederick Canc Res & Dev Ctr, NIH Frederick, MD 21702 USA NCI, Analyt Microscopy Lab, Adv Biosci Labs,Basic Res Program, Frederick Canc Res & Dev Ctr,NIH Frederick, MD 21702 USA Cornell Univ, Med Ctr New York, NY 10021 USA Kureha Chem, Inst Biomed Res Tokyo 160 Japan Shinshu Univ, Sch Med, Dept Mol Biol & Biochem Nagano 3908621 Japan
    1. Year: 2000
  2. Journal: Journal of Biological Chemistry
    1. 275
    2. 18
    3. Pages: 13175-13178
  4. Type of Article: Article
  1. Abstract:

    Nerve growth factor (NGF) stimulation of pheochromocytoma PC12 cells transiently increased the intracellular concentration of reactive oxygen species (ROS). This increase was blocked by the chemical antioxidant N-acetylcysteine and a flavoprotein inhibitor, diphenylene iodonium. NGF responses of PC12 cells, including neurite outgrowth, tyrosine phosphorylation, and AP-1 activation, was inhibited when ROS production was prevented by N-acetylcysteine and diphenylene iodonium. The expression of dominant negative Rac1N17 blocked induction of both ROS generation and morphological differentiation by NGF. The ROS produced appears to be H2O2, because the introduction of catalase into the cells abolished NGF-induced neurite outgrowth, ROS production, and tyrosine phosphorylation, These results suggest that the ROS, perhaps H2O2, acts as an intracellular signal mediator for NGF-induced neuronal differentiation and that NGF-stimulated ROS production is regulated by Rac1 and a flavoprotein-binding protein similar to the phagocytic NADPH oxidase. [References: 26]

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