DNA Fragmentation Induced in High-Cell-Density Culture of Primary Rat Hepatocytes In an Active Process Dependent on Energy Availability, Gene Expression, and Calmdulin

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  • MAEDA Sumio
    Department of Chemistry, National Industrial Research Institute of Nagoya
  • SUZUKI Akemi
    Department of Chemistry, National Industrial Research Institute of Nagoya
  • LIN Kong-Hua
    Department of Chemistry, National Industrial Research Institute of Nagoya
  • INAGAKI Hidetoshi
    Department of Chemistry, National Industrial Research Institute of Nagoya
  • SAITO Takao
    Department of Chemistry, National Industrial Research Institute of Nagoya

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We previously reported that internucleosomal DNA fragmentation, a biochemical feature of apoptosis, was induced spontaneously in high-cell-density culture of adult rat hepatocytes. To understand better the intracellular mechanism of the DNA fragmentation in this system, we have examined the effects of several inhibitors of specific intracellular functions on the DNA fragmentation. We found that the DNA fragmentation could be suppressed by treatment of the cells with inhibitors of mitochondrial respiration, KCN and CCCP, or a protein synthesis inhibitor, cycloheximide. We also demonstrated that calmodulin inhibitors, chlorpromazine and W-7, could suppress the DNA fragmentation. Together, these results lead us to conclude that the DNA fragmentation in hepatocytes cultured at high cell density is an active process dependent on energy availability, gene expression, and calmodulin, rather than a passive event resulting from necrosis. However, by analyzing the incidence of apoptotic morphology during culture, we found that only 2-3% of cells exhibited apoptotic morphology, while the incidence of DNA fragmentation was estimated to be much higher. Based on these results, we estimated that the DNA fragmentation may result from the incomplete progression of apoptosis or from the occurrence of another type of active cell death.

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