Why the study?
Does repeated daunorubicin administration induce MMP activity and cardiac remodeling in a rabbit model of cardiomyopathy?
Does repeated daunorubicin administration induce MMP activity and cardiac remodeling in a rabbit model of cardiomyopathy?
Daunorubicin-induced cardiomyopathy in rabbits is associated with increased myocardial necrosis, fibrosis, and a slight upregulation of MMP-2 activity.
May link daunorubicin to MMP-2 upregulation and fibrosis in rabbits; leaves open translational relevance to clinical cardiomyopathy.
Matrix metalloproteinases (MMPs), activated by oxidative stress, play a key role during cardiac remodeling. In the present study we aimed to assess the role of MMPs in experimental cardiomyopathy induced by repeated 10-week administration of daunorubicin (3 mg/kg i.v.) to rabbits. In the daunorubicin group, the plasma cardiac troponin T levels (cTnT - a marker of myocardial necrosis) were significantly increased (p<0.05), commencing with the 8th administration compared with the controls. The amount of collagen (an estimate of fibrosis) was also significantly higher in the daunorubicin group (13.39 +/- 0.97 mg/g wet weight) compared to the control group (10.03 +/- 0.65 mg/g wet weight). In both groups, the LV MMP-activity was observed only in the gelatine substrate in the 70 kDa region (MMP-2), while no MMPs activities were detectable either in the casein or collagen containing zymograms. At the end of the experiment, the MMP-2 activity was slightly up-regulated (by 16 %) compared with the controls.
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Potáčová et al. (2007) studied this question.
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