Cardiomyocyte survival and DNA reparation in myocardium of C57Bl/6 and mdx mice after dynamical stress

The cardiomyocytes of mdx mice are the prospective model of research on the survival of terminally differentiated cardiomyocytes and the formation of cardiomyopathy in conditions of oxidative stress. Previously, it was observed that dynamical stress induces the formation of low-molecular fragments of DNA. It is beyond questioning that DNA fragmentation develops through the formation of double-strand breaks in DNA (DNA DSB). To record the appearance and disappearance of DSB DNA in the cardiomyocytes of mdx mice after dynamic stress, the antibodies were applied to the phosphorylated form of an H2Ax histon (γ-H2Ax). In the absence of stress, DSB DNA were detected in the nuclei of cells of the myocardium for C57Bl/6 mice (0.05%) and for mdx mice (6.7%), accordingly. For C57Bl mice, 1 h after stress, the share of marked cardiomyocyte nuclei increased up to 1% and, for mdx mice, up to 41.7%. 24 h after stress, in the myocardium of mdx mice, 5.2% of cardiomyocytes in the nuclei were stained, while, for C57BL/6 mice, marked cardiomyocytes in the nuclei were not determined. 24 h after stress, the cell loss of cardiomyocytes for mdx mice was 2.39–2.50%. For C57Bl mice, the general level of cell loss did not exceed a threshold of 0.38%. The obtained data allow us to suspect that, during the survival of cardiomyocytes in mdx mice, a mechanism of DNA reparation is involved.