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

Abstract

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.

• Authors: M Miyamoto, C Kishimoto, K Shioji, H Nakamura, S Toyokuni, Y Nakayama, M Kita, J Yodoi, S Sasayama
• Journal: Japanese circulation journal (Jpn Circ J) Vol. 65 Issue 6 Pg. 561-4 (Jun 2001) ISSN: 0047-1828 [Print] Japan
• PMID: 11407741 (Publication Type: Journal Article)

Chemical References

• Thioredoxins

Topics

• Animals
• Coxsackievirus Infections (etiology, metabolism)
• Disease Models, Animal
• Immunohistochemistry
• Male
• Mice
• Mice, Inbred Strains
• Myocarditis (etiology, metabolism, virology)
• Myocardium (chemistry, pathology)
• Oxidation-Reduction
• Oxidative Stress
• Survival Rate
• Thioredoxins (biosynthesis, metabolism)
• Up-Regulation