Apoptosis is mediated by cytosolic phospholipase A₂ during simulated ischaemia/reperfusion-induced injury in neonatal cardiac myocytes

Abstract 

It has become increasingly clear that apoptosis plays a major role in ischaemia/reperfusion (I/R)-induced cell death, but the molecular basis of this process remains to be elucidated. Therefore, the aim of this study was to investigate the role of cPLA₂ in MAPK phosphorylation and apoptosis in simulated ischaemia/reperfusion (SI/R)-induced injury in neonatal cardiomyocytes. Inhibition of cPLA₂ with AACOCF₃ significantly improved cell viability during SI/R (60.17±1.77 to 80.17±1.97%, p<0.05). The increase in cell viability was associated with a significant inhibition of p38 phosphorylation (135.3±4.47% to 87.94±10.71%, p<0.001) as well as with a significant decrease in caspase-3- (320.32±17.32% to 146.7±28.69%, p<0.01) and PARP-(263.9±8.15% to 154.7±2.24%, p<0.001) cleavage during SI/R. This study provides evidence for a role for cPLA₂ during SI/R-induced injury. It appears that p38 MAPK is a central role player in the signalling pathway involved.