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

Miyamoto, Michiko; Kishimoto, Chiharu; Shioji, Kosei; Nakamura, Hajime; Toyokuni, Shinya; Nakayama, Yasushi; Kita, Masakazu; Yodoi, Junji; Sasayama, Shígetake

doi:10.1253/jcj.65.561

Cited by 14 publications

(15 citation statements)

References 16 publications

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“…38 In vivo studies have also demonstrated that elevated levels of TRX in circulation, caused by either stimulated release of TRX-1 in TRX-1-transgenic mice or intravenous injection of TRX-1, block neutrophil chemotaxis induced by lipopolysaccharide or chemokines. 4,7,31,35,39 Interestingly, these findings are consistent with the report that elevated levels of the classic chemokine interleukin-8 blocked the extravasation of leukocytes into inflammatory sites. 40 Taken together, it is likely that TRX-1 has an immunomodulatory effect in immune responses, which may be due to its chemokine-like activity in inhibiting the recruitment of leukocytes.…”

Section: Discussionsupporting

confidence: 90%

“…We reported previously that myocardial expression and/or serum levels of TRX-1 were increased in patients, rats, and susceptible mouse strains with myocarditis. 25,[33][34][35] To examine whether endogenous TRX-1 is involved in the attenuation of EAM, we used anti-mouse TRX-1 antibody to neutralize the endogenous TRX-1. The neutralization of TRX-1 resulted in a marked enhancement of EAM, whereas control serum had no such effect ( Figure 1A, 1B).…”

Section: Trx-1 Attenuates Autoimmune Myocarditismentioning

confidence: 99%

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Thioredoxin-1 Ameliorates Myosin-Induced Autoimmune Myocarditis by Suppressing Chemokine Expressions and Leukocyte Chemotaxis in Mice

et al. 2004

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Background-Cardiac myosin-induced myocarditis is an experimental autoimmune myocarditis (EAM) model used to investigate autoimmunological mechanisms in inflammatory heart diseases and resembles fulminant myocarditis in humans. We investigated the therapeutic role of thioredoxin-1 (TRX-1), a redox-regulatory protein with antioxidant and antiinflammatory effects, in murine EAM. Methods and Results-EAM was generated in 5-week-old male BALB/c mice by immunization with porcine cardiac myosin at days 0 and 7. Recombinant human TRX-1 (rhTRX-1), C32S/C35S mutant rhTRX-1, or saline was administered intraperitoneally every second day from day 0 to 20. In addition, rabbit anti-mouse TRX-1 serum or normal rabbit serum was administered intraperitoneally on days Ϫ1, 2, and 6. Animals were euthanized on day 21. Histological analysis of the heart showed that TRX-1 significantly reduced the severity of EAM, whereas mutant TRX-1 failed to have such an effect, and anti-TRX-1 antibody enhanced the disease markedly. Immunohistochemical analysis showed that TRX-1 significantly suppressed cardiac macrophage inflammatory protein (MIP)-1␣, MIP-2, and 8-hydroxydeoxyguanosine expression and macrophage infiltration into the heart in EAM. Although serum levels of MIP-1␣ were not suppressed by TRX-1 until day 21, both an in vitro chemotaxis chamber assay and an in vivo air pouch model showed that TRX-1 significantly suppressed MIP-1␣-or MIP-2-induced leukocyte chemotaxis. However, real-time reverse transcription-polymerase chain reaction showed that TRX-1 failed to decrease chemokine receptor expression increased in the bone marrow cells of EAM mice. Conclusions-TRX-1 attenuates EAM by suppressing chemokine expressions and leukocyte chemotaxis in mice.

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Section: Discussionsupporting

confidence: 90%

Section: Trx-1 Attenuates Autoimmune Myocarditismentioning

confidence: 99%

Thioredoxin-1 Ameliorates Myosin-Induced Autoimmune Myocarditis by Suppressing Chemokine Expressions and Leukocyte Chemotaxis in Mice

et al. 2004

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“…The induction of TRX in the lesions might be a nonspecific, secondary phenomenon due to necrosis and inflammation, as shown our previous works [12,23,24]. Also, it was reported that TRX has the function of redox regulation of the transcription factors such as NF-nB or activator protein-1 [9,10].…”

Section: Discussionsupporting

confidence: 55%

“…our study provided the in vivo evidence that the redox regulatory protein, TRX, was upregulated in spontaneous myocardial lesions and that the degree of the upregulation depended upon the severity of the lesions in different strains of mice. TRX per se and the cellular redox state controlled by TRX may play an important role in the pathogenesis and development of the myocardial diseases, as shown in the previous studies [23,24].…”

Section: Discussionmentioning

confidence: 69%

Thioredoxin, a redox-regulating protein, is expressed in spontaneous myocarditis in inbred strains of mice

Miyamoto

Kishimoto

Nimata

et al. 2004

International Journal of Cardiology

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“…Miyamoto et al (51,52) reported strain-dependent predisposition to viral myocarditis and spontaneous myocarditis in mice. Coxsackievirus B3 infection induced severe myocarditis in DBA/2 mice, moderate myocarditis in BALB/c mice, and mild myocarditis in C57BL/6 mice.…”

Section: Thioredoxin As a Biomarker Of Myocarditismentioning

confidence: 99%

From Oxygen Sensing to Heart Failure: Role of Thioredoxin

Hoshino

Shioji

Nakamura

et al. 2007

Antioxidants & Redox Signaling

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Oxidative stress has been widely recognized to be involved in the pathogenesis of cardiopulmonary disorders. In ischemic heart diseases, it is involved not only in the development of atherosclerosis but also in ongoing ischemic injury, especially in the reperfusion process. Cardiomyopathy is another cardiac disorder in which oxidative stress is involved. In diabetic cardiomyopathy, homocysteine, a well-known source of oxidative stress, is believed to play major roles in its development. Thioredoxin (TRX) is a redox-acting protein ubiquitously present in the human body. It also is inducible by a wide variety of oxidative stresses. TRX is a multifunctional protein and has anti-inflammatory and antiapoptotic effects, as well as antioxidative effects. It is therefore feasible to think that TRX is a potential therapy for cardiac disease. Moreover, serum TRX is a well-recognized biomarker of various diseases involving oxidative stress, and this is also the case for cardiac disorders. Here we discuss how TRX is useful as a biomarker of and therapeutic agent for cardiopulmonary disorders, especially focusing on ischemic heart disease, myocarditis and oxygen sensing, and acute respiratory distress syndrome.

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

Cited by 14 publications

References 16 publications

Thioredoxin-1 Ameliorates Myosin-Induced Autoimmune Myocarditis by Suppressing Chemokine Expressions and Leukocyte Chemotaxis in Mice

Thioredoxin-1 Ameliorates Myosin-Induced Autoimmune Myocarditis by Suppressing Chemokine Expressions and Leukocyte Chemotaxis in Mice

Thioredoxin, a redox-regulating protein, is expressed in spontaneous myocarditis in inbred strains of mice

From Oxygen Sensing to Heart Failure: Role of Thioredoxin

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