Ischemic preconditioning activates AMPK in a PKC-dependent manner and induces GLUT4 up-regulation in the late phase of cardioprotection

doi:10.1016/j.cardiores.2003.10.022

Cardiovascular Research 2004 61(3):610-619; doi:10.1016/j.cardiores.2003.10.022
© 2004 by European Society of Cardiology

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Ischemic preconditioning activates AMPK in a PKC-dependent manner and induces GLUT4 up-regulation in the late phase of cardioprotection

Yasuhiro Nishino^a, Tetsuji Miura^*^,a, Takayuki Miki^a, Jun Sakamoto^a^,b, Yuichi Nakamura^a, Yoshihiro Ikeda^a, Hironori Kobayashi^a and Kazuaki Shimamoto^a

^aSecond Department of Internal Medicine, Sapporo Medical University School of Medicine, South-1 west-1, Chou-ku Sapparo 060-8543, Japan
^bDepartment of Pharmacology Sapporo Medical University School of Medicine South-1 west-1, Chou-ku Sapparo 060-8543, Japan

^* Corresponding author. Tel. :+81-11-611-2111; fax: +81-11-644-7958. miura{at}sapmed.ac.jp

Objective: The aim of this study was to determine the role ofAMP-activated protein kinase (AMPK) and its link to proteinkinase C (PKC) in the late phase of cardioprotection affordedby ischemic preconditioning (PC) against myocardial stunning.Methods and results: Rabbits were instrumented with a balloonoccluder around a coronary artery and with a Doppler sensorto monitor the thickening fraction (TF). Conscious rabbits underwentfive cycles of 5-min ischemia/5-min reperfusion (I/R) on 2 consecutivedays (days 1 and 2). Reduction of TF after I/R was significantlyless and recovery of TF was faster on day 2, indicating a latePC effect. PC provoked translocation of PKC- ${varepsilon}$ from the cytosolto the membrane and significantly increased AMPK activity by100% immediately after PC. The mRNA level of GLUT4, a glucosetransporter, was elevated by 150% at 3 h after PC, and the totalprotein level of GLUT4 was increased by 107% at 24 h after PC.The level of sarcolemmal GLUT4 protein after I/R on day 2 was41% higher than its level after I/R on day 1. AMPK activationand up-regulation of GLUT4 by PC were abrogated by pre-treatmentwith PKC inhibitors. Conclusion: PC activated AMPK and up-regulatedGLUT4 expression in a PKC-dependent manner. This GLUT4 up-regulationat 24 h after PC may contribute to attenuation of myocardialstunning.

KEYWORDS Ischemia; Preconditioning; Protein kinases; Stunning

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