Fig. 6 | Nature Communications

Fig. 6

From: DNA damage-induced PARP1 activation confers cardiomyocyte dysfunction through NAD+ depletion in experimental atrial fibrillation

Fig. 6

The PARP inhibitor ABT-888 attenuates tachypacing-induced PARP1 activation, NAD+ depletion and CaT loss in adult rat atrial cardiomyocytes. ad Representative Western blot and quantified data of PAR, PARP1, and γH2AX expression levels in rat atrial cardiomyocytes. Tachypacing (TP) significantly increased PAR levels, which was inhibited by the PARP inhibitor ABT-888. PARP1 protein levels were not changed by TP. TP significantly increased DNA damage (γH2AX) compared to NP. *P < 0.05 vs. control (CTL) NP, n = 3 independent experiments. e TP reduced NAD+ levels, which was prevented by PARP inhibitor ABT-8888. ***P < 0.001 vs. CTL NP ##P < 0.01 vs. CTL TP, n = 4 independent experiments. f, g Representative CaT traces and quantified CaT amplitude in control normal-paced (NP) or TP rat atrial cardiomyocytes pretreated with ABT-888 or vehicle DMSO (CTL). ***P < 0.001 vs. CTL NP, ###P < 0.001 vs. CTL TP, n = 79 cardiomyocytes for CTL NP, n = 61 for ABT-888 NP, n = 63 for CTL TP, n = 57 for CTL TP. Data are all expressed as mean ± s.e.m. Individual group mean differences were evaluated with the two-tailed Student’s t test

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