Kawamura S, Yoshida K, Miura T, Mizukami Y, Matsuzaki M
Department of Internal Medicine, Yamaguchi University School of Medicine, Yamaguchi 755-8505, Japan.
Am J Physiol. 1998 Dec;275(6):H2266-71. doi: 10.1152/ajpheart.1998.275.6.H2266.
Protein kinase C (PKC) plays an important role in mediating ischemic preconditioning (PC). However, the relationship between PKC isoforms and PC is still uncertain. We analyzed subcellular localization of PKC isoforms by Western blot analysis in isolated rat heart and demonstrate that PKC-alpha, -delta, and -epsilon were translocated to the membrane fraction associated with the improvement of cardiac function. Translocation of PKC-delta and -epsilon persisted after a 30-min period following PC, but the translocation of PKC-alpha was transient. Under low Ca2+ perfusion (0.2 mmol/l), PC improved the cardiac function associated with the translocation of PKC-delta. Chelerythrine (1.0 micromol/l) suppressed the translocation of all PKC isoforms associated with the loss of improvement of the cardiac function. On the other hand, bisindolylmaleimide (0.1 micromol/l) did not inhibit the improvement of cardiac function induced by PC, which was associated with the translocation of PKC-epsilon. These results indicate that the effect of PC on cardiac function is mediated by the translocation of either PKC-delta or -epsilon independently in rat hearts.
蛋白激酶C（PKC）在介导缺血预处理（PC）中起重要作用。然而，PKC同工型与PC之间的关系仍不明确。我们通过蛋白质印迹分析在离体大鼠心脏中分析了PKC同工型的亚细胞定位，结果表明PKC-α、-δ和-ε转位至与心脏功能改善相关的膜组分。PKC-δ和-ε的转位在PC后30分钟内持续存在，但PKC-α的转位是短暂的。在低钙灌注（0.2 mmol/L）条件下，PC改善心脏功能与PKC-δ的转位相关。白屈菜红碱（1.0 μmol/L）抑制了所有PKC同工型的转位，这与心脏功能改善的丧失相关。另一方面，双吲哚马来酰胺（0.1 μmol/L）并未抑制PC诱导的心脏功能改善，这与PKC-ε的转位相关。这些结果表明，在大鼠心脏中，PC对心脏功能的影响是由PKC-δ或-ε的转位独立介导的。
