Extracellular Matrix Remodeling in Coxsackievirus B3 Myocarditis

Kishimoto, Chiharu; Kitazawa, Mikio; Hiraoka, Yuji; Takada, Hitoshi

doi:10.1006/clin.1997.4418

Cited by 9 publications

(2 citation statements)

References 29 publications

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“…The coxsackievirus B3 (CVB3) used in this study was derived from the infectious cDNA copy of the cardiotropic H3 strain (Woodruff variant) of CVB3 (24). Virus titers were determined on HeLa cell monolayers using a standard plaque-forming assay, and virus isolation from heart and liver was performed as described previously (25). Recombinant adenovirus vectors containing the genes for LacZ, Myc-tagged SOCS1, Myc-tagged SOCS3, and Cre recombinase were prepared on 293 cells as described previously (26).…”

Section: Methodsmentioning

confidence: 99%

The suppressor of cytokine signaling–1 (SOCS1) is a novel therapeutic target for enterovirus-induced cardiac injury

Yasukawa¹,

Yajima²,

Duplain³

et al. 2003

J. Clin. Invest.

112

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Section: Methodsmentioning

confidence: 99%

The suppressor of cytokine signaling–1 (SOCS1) is a novel therapeutic target for enterovirus-induced cardiac injury

Yasukawa¹,

Yajima²,

Duplain³

et al. 2003

J. Clin. Invest.

112

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“…On the day of assay, the frozen tissue was homogenized in 200 l of PBS and centrifuged at 12,000 rpm for 5 min. Viral titer (expressed in PFU) was determined in the supernatants by a plaque assay method on HeLa cell monolayers as previously described (12).…”

Section: Plaque-forming Assay Determination Of Cardiac Viral Loadmentioning

confidence: 99%

Antiviral and myocyte protective effects of murine interferon-β and -α₂in coxsackievirus B3-induced myocarditis and epicarditis in Balb/c mice

Wang¹,

Cunha²,

Vincelette³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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The present study tested the hypothesis that murine (m)IFN-beta or mIFN-alpha(2) can eliminate cardiac viral load and protect cardiomyocytes from injury in animals infected with coxsackievirus B3 (CVB3). CVB3-inoculated male Balb/c mice exhibited signs of illness, including lethargy, progressive weight loss, and death (10% on day 3 and 100% on day 8). Cardiac viral load was high [4,277 +/- 1,009 plaque-forming units and 25 +/- 5 copies CVB3/hypoxanthine guanine phosphoribosyl transferase 1 mRNA] on day 4. The cardiac tissue exhibited severe inflammatory infiltration and myocyte damage with an average myocarditis integrated pathology score of 2.1 +/- 0.2 on day 7. Most of the mice infected with CVB3 also developed epicarditis, and 55% had intraventricular thrombi present. Treatment with mIFN-beta [2.5 to 10 million international units (MIU)/kg] dose-dependently improved the general health status in CVB3-inoculated mice, as evidenced by reduction in weight loss, prevention of death, elimination of cardiac viral load, protection of myocytes from injury, decrease in inflammatory cell infiltration, and attenuation of intraventricular thrombus formation. Treatment with 10 MIU/kg mIFN-alpha(2) resulted in a similar level of efficacy as that induced by 5 MIU/kg mIFN-beta, with the exception that mIFN-alpha(2) did not reduce cardiac CVB3 mRNA. However, mIFN-alpha(2) , but not any dose group of mIFN-beta, significantly attenuated CVB3-induced epicarditis. These data demonstrate antiviral effects for both mIFN-beta and mIFN-alpha(2), which lead to protection of the mice from CVB3-induced myocarditis. However, the potential mechanisms leading to a differential host response for the two isoforms of mIFN remain to be elucidated.

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Myocardial Proteases and Matrix Remodeling in Acute Myocarditis and Inflammatory Cardiomyopathy

Rutschow

Noutsias

Pauschinger

2010

Inflammatory Cardiomyopathy (DCMi)

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Extracellular Matrix Remodeling in Coxsackievirus B3 Myocarditis

Cited by 9 publications

References 29 publications

The suppressor of cytokine signaling–1 (SOCS1) is a novel therapeutic target for enterovirus-induced cardiac injury

The suppressor of cytokine signaling–1 (SOCS1) is a novel therapeutic target for enterovirus-induced cardiac injury

Antiviral and myocyte protective effects of murine interferon-β and -α₂in coxsackievirus B3-induced myocarditis and epicarditis in Balb/c mice

Myocardial Proteases and Matrix Remodeling in Acute Myocarditis and Inflammatory Cardiomyopathy

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Extracellular Matrix Remodeling in Coxsackievirus B3 Myocarditis

Cited by 9 publications

References 29 publications

The suppressor of cytokine signaling–1 (SOCS1) is a novel therapeutic target for enterovirus-induced cardiac injury

The suppressor of cytokine signaling–1 (SOCS1) is a novel therapeutic target for enterovirus-induced cardiac injury

Antiviral and myocyte protective effects of murine interferon-β and -α2in coxsackievirus B3-induced myocarditis and epicarditis in Balb/c mice

Myocardial Proteases and Matrix Remodeling in Acute Myocarditis and Inflammatory Cardiomyopathy

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Product

Resources

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Antiviral and myocyte protective effects of murine interferon-β and -α₂in coxsackievirus B3-induced myocarditis and epicarditis in Balb/c mice