Difference in Thioredoxin Expression in Viral Myocarditis in Inbred Strains of Mice

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  • Miyamoto Miki
    Department of Cardiovascular Medicine, Graduate School of Medicine
  • Kishimoto Chiharu
    Department of Cardiovascular Medicine, Graduate School of Medicine
  • Shioji Keisuke
    Department of Cardiovascular Medicine, Graduate School of Medicine
  • Nakamura Hajime
    Department of Biological Responses, Institute for Virus Research
  • Toyokuni Shinya
    Department of Pathology and Biology of Diseases, Graduate School of Medicine, Kyoto University
  • Nakayama Yukie
    Department of Cardiovascular Medicine, Graduate School of Medicine
  • Kita Masakazu
    Department of Microbiology, Kyoto Prefectural Medical University
  • Yodoi Junji
    Department of Biological Responses, Institute for Virus Research
  • Sasayama Shigetake
    Department of Cardiovascular Medicine, Graduate School of Medicine

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Redox regulating mechanisms may be involved in the pathogenesis of viral myocarditis and thioredoxin (TRX) is a small multifunctional protein that contains a redox active sequence. The present study investigated the histopathology and characteristics of TRX expression in acute coxsackievirus B3 myocarditis in inbred strains of mice (severe myocarditis in DBA/2 mice, moderate myocarditis in BALB/c mice and mild myocarditis in C57BL/6 mice). Thioredoxin was upregulated and its expression correlated with the severity of the disease. In addition, 8-hydroxy-2'-deoxyguanosine, which is an established marker for oxidative stress, was concominantly positive in damaged myocytes. Thus, TRX may be specifically induced by the acute inflammatory stimuli in murine viral myocarditis, and the severity and development of acute viral myocarditis may be regulated by the cellular redox state. (Jpn Circ J 2001; 65: 561 - 564)

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