Fig. 5: PARP1-mediated autophagy promotes cardiomyocyte death through FoxO3a pathway.

Primary neonatal rat cardiomyocytes were treated with PJ34 (10 μM), or infected with PARP1 shRNA, and then starved for 24 h. a Cell viability was determined by MTT colorimetric assay. b Cells were labeled with PI/Annexin V and analysed by fluorocytometry. N = 5 for each group. ^**P < 0.01 vs. control; ^##P < 0.01 vs. starve or starve + scramble shRNA. c and d After infection with FoxO3a shRNA for 24 h, cardiomyocytes were infected with Ad-PARP1 for 24 h and were then exposed to starvation for 24 h. Cell viability (c) and PI/Annexin V-labeled apoptosis cells (d) were accessed. N = 5 for each group.^**P < 0.01 vs. control; ^##P < 0.01 vs. starve; ^$$P < 0.01 vs. starve + Ad-PARP1. e and h cells were first infected with Histone H1 shRNA, and treated with PJ34 or PARP1 shRNA and then exposed to starvation for 24 h. Cell viability (e and g) and PI/Annexin V-labeled apoptosis cells (f and h) were accessed. N = 5 for each group. ^**P < 0.01 vs. control; ^##P < 0.01 vs. starve; ^$$P < 0.01 vs. starve + PJ34 or starve+PARP1 shRNA