Upregulation of thioredoxin (TRX) expression in giant cell myocarditis in rats

K Shioji, C Kishimoto, H Nakamura, S Toyokuni… - FEBS …, 2000 - Wiley Online Library
K Shioji, C Kishimoto, H Nakamura, S Toyokuni, Y Nakayama, J Yodoi, S Sasayama
FEBS letters, 2000Wiley Online Library
To examine the possible involvement of a redox regulating mechanism in the pathogenesis
of immune‐mediated myocarditis, myocarditis was induced by immunization of porcine
cardiac myosin in rats and immunohistochemistry and Western blot for thioredoxin (TRX)
were performed. Immunohistochemistry for 8‐hydroxy‐2′‐deoxyguanosine (8‐OHdG) and
nuclear factor kappa‐B (NF‐κB) was also performed. TRX was upregulated in the acute
stage, but not in the chronic stage, and the expression was correlated with the severity of the …
To examine the possible involvement of a redox regulating mechanism in the pathogenesis of immune‐mediated myocarditis, myocarditis was induced by immunization of porcine cardiac myosin in rats and immunohistochemistry and Western blot for thioredoxin (TRX) were performed. Immunohistochemistry for 8‐hydroxy‐2′‐deoxyguanosine (8‐OHdG) and nuclear factor kappa‐B (NF‐κB) was also performed. TRX was upregulated in the acute stage, but not in the chronic stage, and the expression was correlated with the severity of the disease. Damaged myocytes were strongly immunostained for 8‐OHdG and NF‐κB. Thus, TRX may be specifically induced by acute inflammatory stimuli, and the development of acute immune‐mediated myocarditis may be regulated by the cellular redox state via TRX.
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