Figure 2

Rapid activation of PARP-1 in peripheral leukocytes induced after recanalization of the infarct-related coronary artery by primary PCI. (A) Densitometry analysis of PAR Western blots performed on patient leukocytes. (C) Immunohistochemical PAR-score analysis of patient leukocytes. In both figures, lane 1 indicates densitometry units (A) or PAR-score values (C) in stable angina patients before coronarography; lanes 2–5 show PAR content in control patients with elective PCI before coronarography (lane 2), immediately after the successful PCI (lane 3), 24 ± 4 h after (lane 4), and 96 ± 4 h after PCI (lane 5); lanes 6–9 indicate PAR content in patients with acute myocardial infarction before coronarography (lane 6), immediately after the successful PCI (lane 7), 24 ± 4 h after reperfusion of the ischemic myocardium (lane 8), and 96 ± 4 h after PCI (lane 9). Primary PCI leads to a significant increase in leukocyte cellular PAR content, reflecting rapid activation of PARP during reperfusion. A gradual decrease of PARP activity can be observed at 24- and 96-h time points after myocardial infarction. PARP activity is not affected during elective PCI. Results are expressed as mean (represented by squares) ± SEM (represented by boxes) and ± SD (represented by bars). (B) Representative examples of PAR Western blots from 3 stable angina patient leukocytes as controls (first panel) and 3 STEMI patients (second panel). Time points are indicated. Commercially available PARP enzyme served as a positive control. *P< 0.05, NS, nonsignificant.