The study provides preclinical evidence that specific PKC isozymes translocate to the nucleus and increase nuclear protein phosphorylation during myocardial ischemia and reperfusion.
Should not alter clinical management; hypothesis-generating for PKC isozyme roles in myocardial ischemia-reperfusion.
Protein kinase C (PKC) has been suggested to mediate, at least in part, multiple processes in the pathophysiological sequelae of myocardial ischemia. The present study demonstrates that the epsilon, eta and iota isozymes of PKC are translocated to nuclei in response to brief intervals of global ischemia as well as reperfusion of ischemic rat myocardium. Concomitant with the translocation of PKC isozymes to nuclei during ischemia, increased PKC-mediated nuclear protein phosphorylation was observed. Taken together, the present results demonstrate that nuclear signaling mechanisms are activated during myocardial ischemia that include PKC translocation and PKC-mediated nuclear protein phosphorylation.
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Albert et al. (1998) studied this question.
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