Differential effect of ischemic and pharmacological preconditioning on PKC isoform translocation in adult rat cardiac myocytes

The role of PKC isoforms in the protection of ischemic preconditioning remains controversial. The aim of the present study was to compare PKC translocation in ischemic and pharmacological preconditioning and to test the hypothesis that induction of the preconditioned state results in a sustained translocation of PKC during the following ischemic period. Isolated rat cardiac myocytes were subjected to established preconditioning protocols using either transient ischemia or (xi-adrenergic stimulation. Translocation of PKC isoforms, -alpha, -delta and -epsilon to the particulate fraction during induction of preconditioning, post incubation or final sustained ischemia was assessed by immunoblotting. Ischemia alone caused the translocation of PKC-alpha and -epsilon, from the soluble to the particulate fraction. All three PKC isoforms examined were translocated to the particulate fraction in response to stimulation with (Xi-adrenergic agonists, or phorbol esters. Ischemic preconditioning resulted in the translocation of only the PKC-epsilon isoform while pharmacological preconditioning did not affect any of the isoforms. During the following sustained ischemic period, increased percentage of PKC-alpha and -epsilon isoforms associated with the particulate fraction was observed only for the pharmacologically preconditioned cells. It is concluded that PKC translocation during preconditioning or the following ischemic period is not essential for the mediation of protection of rat cardiomyocytes in vitro. Copyright (C) 2002 S. Karger AG, Basel.