Histone hyperacetylation is independent of cell death.

<p>In (A and B), cardiac myocytes were pretreated with mitochondrial permeability transition pore (mPTP) inhibitor TAT-BH4, before exposure to hypoxia or HA, and histone acetylation or DNA fragmentation measured as described in Methods. In (C and D), cardiac myocytes exposed to hypoxia (HX) or hypoxia-acidosis (HA) in the presence and absence of the mPTP inhibitor cyclosporine A (CsA), the caspase inhibitor BocD, or the calpain inhibitor calpeptin as indicated. Western blot quantitation of histone H3 acetylation in the presence of BocD and calpeptin (Cal) is shown in (E). In (F and G) cardiac myocytes were treated with vehicle (UT), or with staurosporine or hydrogen peroxide (H₂O₂) as indicated, to induce cell death, and the acetylation level of histone H3 was determined by western blot analysis. As a positive control for histone acetylation cardiac myocytes were also treated with the HDAC inhibitor TSA. The effect of staurosporine (ST) treatment on histone H3 and H4 acetylation is shown in (H). All results are mean ± S.E.M., n = 3.