Fig. 1
From: Myocardial Postischemic Injury Is Reduced by PolyADPribose Polymerase-1 Gene Disruption
Basal polyADPribosylation in brain, pancreas and heart, and PARP activation in heart after I/R.
WT brain and pancreas show comparable levels of basal PARP activity, with negligible polyADPribosylation in PARP-1−/− brain and pancreas, (p < 0.001). Sham-treated WT heart shows roughly twice the amount of basal PARP activity as WT brain and pancreas (p < 0.001), and polyADPribosylation is augmented by 30% following I/R (p < 0.01). WT heart PARP activity is decreased to approximately 50% of baseline levels when the superoxide dismutase (SOD) analog SC-55858 (40 µM) or the NOS inhibitor L-NAME (1mM) are included in the reperfusion phase (p < 0.001). Unlike PARP-1/- brain or pancreas, sham-treated PARP-1−/− heart contains approximately 65% of basal polyADPribosylation seen in sham-treated WT hearts (p < 0.01). PolyADPribosylation in PARP-1−/− hearts is augmented by 60% with I/R (p < 0.001). WT, wild type; PARP, polyADPribose polymerase; I/R, ischemia-reperfusion.