ABSTRACT
BACKGROUND: The pathogenesis of transition from viral myocarditis to dilated cardiomyopathy is elusive, although the incidence of dilated cardiomyopathy in human is increasing. METHODS: To clarify the role of the tissue inhibitor of matrix metaloproteinase-2 (TIMP-2) in this event, we performed immunohistochemistry, immunoblotting and immunoassay of matrix metalloproteinase-9 (MMP-9) and TIMP-2 in the serum and heart tissue of mice, which were inoculated with 4000 plaque-forming units of coxsackie B virus. RESULTS: The MMP-9 was expressed in damaged cardiomyocytes, and the TIMP-2 was expressed in mainly interstitial connective tissue between cardiac muscle bundles by immunohistochemistry. The level of serum MMP-9 was higher in the complicated than non-complicated group (p<0.001), but the level of TIMP-2 was much lower in complicated than non-complicated group (p<0.05). These findings were similar to the results of immunohistochemistry and immunoblotting in tissues. CONCLUSIONS: These results suggest that an imbalance in the level of MMP-9 and its inhibitor might activate cardiac complication in viral myocarditis.