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J. Biochem, 1997, Vol. 122, No. 3 506-511
© 1997 Japanese Biochemical Society


research-article

Implication of Protein Kinase C-{alpha}, {delta}, and {varepsilon} Isoforms in Ischemic Preconditioning in Perfused Rat Hearts1

Ken-ichi Yoshida*,2, Shuichi Kawamura{dagger}, Yoichi Mizukami* and Masafumi Kitakaze{ddagger}

*Department of Legal Medicine Yamaguchi University School of Medicine Ube, Yamaguchi 755
{dagger}The Second Department of Medicine, Yamaguchi University School of Medicine Ube, Yamaguchi 755
{ddagger}The First Department of Medicine, Osaka University School of Medicine Osaka 565

2To whom correspondence should be addressed

Ischemic preconditioning is a phenomenon in which one or several cycle(s) of brief ischemia-reperfusion protects the myocardium against the cell injury caused by subsequent prolonged ischemia. Protein kinase C (PKC) inhibitors blunt the cardioprotection arising from ischemic preconditioning. To investigate which PKC isoform is involved in ischemic preconditioning, we identified the PKC isoform that translocates to the membrane fraction by means of immunoblotting with specific antibodies. PKC-{alpha}, {delta}, {varepsilon} isoforms all increased in the membrane fraction after three cycles of 3 min ischemia and 5 min reperfusion (ischemic preconditioning) in the perfused rat heart. The ischemic preconditioning significantly improved the recovery of left ventricular developed pressure (LVDP) during reperfusion following 20 min of ischemia. A PKC specific inhibitor, chelerythrine (1.0 µM) blocked the effect of ischemic preconditioning on LVDP recovery and the translocation of PKC-{alpha}, {delta}, {varepsilon} isoforms. These data suggest that one or more of these three isoforms of PKC is involved in ischemic preconditioning by phosphorylating membrane proteins.

1This study was supported by a Grant-in-Aid from the Ministry of Science, Education, Sports and Culture of Japan.


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