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 pre-conditioning protocols using either transient ischemia or α1-adrenergic stimulation. Translocation of PKC isoforms, -α, -δ and -Ε 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-α and -Ε from the soluble to the particulate fraction. All three PKC isoforms examined were translocated to the particulate fraction in response to stimulation with α1-adrenergic agonists or phorbol esters. Ischemic preconditioning resulted in the translocation of only the PKC-Ε isoform while pharmacological precondi-tion-ing did not affect any of the isoforms. During the following sustained ischemic period, increased percentage of PKC-α and -Ε 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.

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© 2002 S. Karger AG, Basel
2002
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