Stress and Redox Regulation. Cell injury and its protection in astrocytes.

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  • MATSUDA Toshio
    Laboratories of Medicinal Pharmacology, Graduate School of Pharmaceutical Sciences, Osaka University
  • TAKUMA Kazuhiro
    Departments of Analytical Chemistry, Faculty of Pharmaceutical Sciences, Kobe Gakuin University
  • LEE Eibai
    Departments of Pharmacology, Faculty of Pharmaceutical Sciences, Kobe Gakuin University
  • BABA Akemichi
    Laboratories of Molecular Neuropharmacology, Graduate School of Pharmaceutical Sciences, Osaka University

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  • ストレスと細胞応答　　グリア細胞の障害と保護
  • グリア サイボウ ノ ショウガイ ト ホゴ
  • ストレスと細胞応答

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Abstract

Incubation of cultured astrocytes in Ca2+-containing medium after exposure to Ca2+-free medium causes Ca2+ influx followed by delayed cell death. Here, we summarize the mechanisms underlying the Ca2+-mediated injury of cultured astrocytes and the protective effects of drugs against Ca2+-reperfusion injury. Our results show that Ca2+-reperfusion injury of astrocytes appears to be mediated by apoptosis as evidenced by DNA fragmentation and nuclear condensation. Calpain, reactive oxygen species (ROS) production, calcineurin, caspase-3, and NF-κB activation are involved in Ca 2+-reperfusion injury. Several drugs including T-588 and idebenone protect astrocytes against Ca2+-reperfusion injury. The protective effect of idebenone is mediated by nerve growth factor production, whereas that of T-588 is mediated mainly by the mitogen-activated protein/extracellular signal-regulated kinase signal cascade.

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