Abstract
Purpose Increasing evidence suggests that human diseased cardiomyocytes have the potential to dedifferentiate. The aim of our research was to monitor the distribution and ratio of dedifferentiation markers in rodent and human cardiomyocytes in order to estimate their potential to serve as diagnostic and prognostic tools. Methods and Materials We studied human heart explants of 35 patients suffering from end-stage heart failure (HF) and 2 healthy controls. For comparison mice were analyzed four, seven and 21 days after myocardial infarction (MI). In addition, we induced dedifferentiation in mice through daily injection of 5 μg oncostatin M (OSM) for two weeks. Morphologic analysis was performed utilizing antibodies specific for α-smooth muscle actin (SMA) and α-smooth muscle actinin (SMAct). Results Injection of OSM induced high expression of several dedifferentiation markers in mice myocardium. Especially the amount of SMA- and SMAct-positive cardiomyocytes increased eight- and ten-fold, respectively (p Conclusions SMA is probably an early marker of injury and dedifferentiation, while SMact characterizes rather chronic processes. Monitoring both markers might help to characterize the progression of the disease status in patients with chronic heart failure.
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