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• W1972130056 abstract "Abstract: Staurosporine (0.03–0.5 µM) induced a dose-dependent, apoptotic degeneration in cultured rat hippocampal neurons that was sensitive to 24-h pretreatments with the protein synthesis inhibitor cycloheximide (1 µM) or the cell cycle inhibitor mimosine (100 µM). To investigate the role of Ca2+ and reactive oxygen species in staurosporine-induced neuronal apoptosis, we overexpressed calbindin D28K, a Ca2+ binding protein, and Cu/Zn superoxide dismutase, an antioxidative enzyme, in the hippocampal neurons using adenovirus-mediated gene transfer. Infection of the cultures with the recombinant adenoviruses (100 multiplicity of infection) resulted in a stable expression of the respective proteins assessed 48 h later. Overexpression of both calbindin D28K and Cu/Zn superoxide dismutase significantly reduced staurosporine neurotoxicity compared with control cultures infected with a β-galactosidase overexpressing adenovirus. Staurosporine-induced neuronal apoptosis was also significantly reduced when the culture medium was supplemented with 10 or 30 mM K+, suggesting that Ca2+ influx via voltage-sensitive Ca2+ channels reduces this apoptotic cell death. In contrast, neither the glutamate receptor agonist NMDA (1–10 µM) nor the NMDA receptor antagonist dizocilpine (MK-801; 1 µM) was able to reduce staurosporine neurotoxicity. Cultures treated with the antioxidants U-74500A (1–10 µM) and N-acetylcysteine (100 µM) also demonstrated reduced staurosporine neurotoxicity. These results suggest a fundamental role for both Ca2+ and reactive oxygen species in staurosporine-induced neuronal apoptosis." @default.
• W1972130056 created "2016-06-24" @default.
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• W1972130056 date "2002-11-18" @default.
• W1972130056 modified "2023-10-15" @default.
• W1972130056 title "Ca2+ and Reactive Oxygen Species in Staurosporine-Induced Neuronal Apoptosis" @default.
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• W1972130056 doi "https://doi.org/10.1046/j.1471-4159.1997.68041679.x" @default.
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