Key result
Treatment with a c-fos monoclonal antibody significantly decreased myocardial necrosis and inflammatory cell infiltration in mice with viral myocarditis compared to normal saline.
Why the study?
Does treatment with a c-fos monoclonal antibody reduce myocardial necrosis and cell infiltration in a mouse model of viral myocarditis?
Does treatment with a c-fos monoclonal antibody reduce myocardial necrosis and cell infiltration in a mouse model of viral myocarditis?
In a mouse model of viral myocarditis, c-fos expression is upregulated and its inhibition with a monoclonal antibody reduces myocardial necrosis and cellular infiltration.
Answers are grounded in this paper and cite their sources.
Does not support clinical use in viral myocarditis; leaves open c-fos inhibition as a translational target.
BACKGROUND: c-fos may play a role in the pathogenesis of some diseases. The expression and function of c-fos in viral myocarditis (VMC) have not yet been reported. To study the change and significance of proto-oncogene c-fos in VMC is the objective of this experiment. METHODS: An animal model of VMC was established via coxsackie virus B3 inoculation. VMC mice were then treated with a c-fos monoclonal antibody and isoproterenol and the protein and mRNA expression of c-fos were studied via immunohistochemical analysis and in situ hybridization. Results were simultaneously analyzed for the significance of c-fos expression in mice with VMC. RESULTS: Myocardial necrosis and cell infiltration decreased after treatment with c-fos monoclonal antibody compared to control mice, while myocardial necrosis and cell infiltration were increased after treatment with isoproterenol. Positive cardiomyocytes with c-Fos expression increased at 3, 5, 7, 9, and 15 days after virus inoculation in VMC mice compared to control mice, while returning to almost normal levels at 35 days. The expression level of c-fos mRNA at 3 and 7 days after virus inoculation in VMC mice was also higher than that of control mice. CONCLUSIONS: c-fos expression in the cardiomyocytes of VMC mice is significantly increased, c-fos plays an important role in myocardial lesions. The apparent increase in expression of c-fos is likely to be involved in the pathogenesis of VMC.
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Zhang et al. (2010) studied Viral myocarditis (n=250). c-fos monoclonal antibody vs. Normal saline was evaluated on Myocardial lesions (infiltration of inflammatory cells score at 7 days) (p=<0.01). Treatment with a c-fos monoclonal antibody significantly decreased myocardial necrosis and inflammatory cell infiltration in mice with viral myocarditis compared to normal saline.
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