Fig. 4

Effects of vorinostat treatment of quiescent SLE-derived cells. Autoradiograms showing micrococcal nuclease sensitivity of the N-ras locus in untreated PBMCs from six healthy controls (HC) (a) and six quiescent systemic lupus erythematosus (QSLE) patients (b), as well as in PBMCs from the same QSLE patients after treatment with 2.5 μM vorinostat for 24 h (c). Symbols M, D and T represent the positions of nucleosome monomer, dimer and trimer respectively. d Western blot analysis of PBMCs from a representative quiescent SLE patient treated with various doses of vorinostat for 24 h. Nonacetylated histone H4 was used as a control for acetylated histone H4, and beta actin as a loading control. The kinetics of monoadducts (e) and γH2AX foci (g) as well as total amounts of monoadducts (f) and γH2AX foci expressed as AUC (h) after treatment of PBMCs from QSLE patients and their matched healthy controls with melphalan in the presence or not of vorinostat. The asterisks indicate significant differences (p < 0.05) between QSLE and LN patients. i The induction of apoptosis after treatment of PBMCs from the same QSLE patients and their matched HC with melphalan in the presence or not of vorinostat. The experiments shown were based on a minimum of three independent repeats and the data reported are the mean ± SD of all the subjects analyzed.