Difference in thioredoxin expression in viral myocarditis in inbred strains of mice

被引:13
作者
Miyamoto, M
Kishimoto, C
Shioji, K
Nakamura, H
Toyokuni, S
Nakayama, Y
Kita, M
Yodoi, J
Sasayama, S
机构
[1] Kyoto Univ, Grad Sch Med, Dept Cardiovasc Med, Sakyo Ku, Kyoto 6068507, Japan
[2] Kyoto Univ, Grad Sch Med, Inst Virus Res, Dept Biol Responses, Kyoto, Japan
[3] Kyoto Univ, Grad Sch Med, Dept Pathol & Biol Dis, Kyoto, Japan
[4] Kyoto Prefectural Univ Med, Dept Microbiol, Kyoto 602, Japan
来源
JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION | 2001年 / 65卷 / 06期
关键词
coxsackievirus B3; oxidative stress; thioredoxin; viral myocarditis;
D O I
10.1253/jcj.65.561
中图分类号
N09 [自然科学史]; B [哲学、宗教];
学科分类号
01 [哲学]; 0101 [哲学]; 010108 [科学技术哲学]; 060207 [中国近代史]; 060305 [世界专门史]; 0712 [科学技术史];
摘要
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.
引用
收藏
页码:561 / 564
页数:4
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