[Cardiomyocyte survival and DNA repair in myocardium from C57Bl/6 and mdx mice after dynamical stress].

Mdx mice cardiomyocytes are a perspective model to study survival of terminally differentiated cardiomyocytes and formation of cardiomyopathy under conditions of oxidative stress. It was previously observed that dynamical stress induced formation of low molecular DNA fragments. It is beyond question that DNA fragmentation develops because of formation of double strand DNA breaks (DNA DSB).

[Double strand DNA breaks in C57B1 and mdx mice cardiomyocytes after dynamical stress].

The survival of cardiac myocytes under different physiological and pathological conditions presents pressing problem. mdx mice cardiac myocytes are a promising model of cell survival under condition of oxidative stress. Our early results have shown that some part of mdx mice cardiomyocytes is in early stage of apoptosis (Kazakov, Mikhailov, 2001).

Slow elimination of phosphorylated histone gamma-H2AX from DNA of terminally differentiated mouse heart cells in situ.

Phosphorylation of replacement histone H2AX occurs in megabase chromatin domains around double-strand DNA breaks (DSBs) and this modification (called gamma-H2AX) may serve as a useful marker of genome damage and repair in terminally differentiated cells. Here using immunohistochemistry we studied kinetics of gamma-H2AX formation and elimination in the X-irradiated mouse heart and renal epithelial tissues in situ. Unirradiated tissues have 3-5% gamma-H2AX-positive cells and in tissues fixed 1h after X-irradiation gamma-H2AX-positive nuclei are induced in a dose-dependent manner approaching 20-30% after 3 Gy of IR.