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Am J Physiol Heart Circ Physiol (March 28, 2002). doi:10.1152/ajpheart.00434.2001
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Articles in PresS, published online ahead of print March 28, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00434.2001
Submitted on May 22, 2001
Accepted on March 26, 2002

Opening of mitochondrial KATP channel occurs downstream of PKC-{epsilon} activation in the mechanism of preconditioning

Yoshito Ohnuma1, Tetsuji Miura1*, Takayuki Miki1, Masaya Tanno1, Atsushi Kuno1, Akihito Tsuchida1, and Kazuaki Shimamoto1

1 Second Department of Internal Medicine, Sapporo Medical University, Sapporo, Japan

* To whom correspondence should be addressed. E-mail: miura{at}sapmed.ac.jp.

We examined whether the mitochondrial KATP channel (mitoKATP) is an effector downstream of protein kinase C-{epsilon} (PKC-{epsilon}) in the mechanism of preconditioning (PC) in isolated rabbit hearts. PC with 2 cycles of 5-min ischemia/5-min reperfusion before 30-min global ischemia reduced infarction from 50.3±6.8% of the left ventricle to 20.3±3.7%. PC significantly increased PKC-{epsilon} protein in the particulate fraction from 51±4% of the total to 60±4%, whereas no translocation was observed for PKC-{delta} and PKC-{alpha}. In mitochondria separated from the other particulate fractions, PC increased the PKC-{epsilon} level by 50%. Infusion of 5-hydroxydecanoate (5-HD), a mitoKATP blocker, after PC abolished the cardioprotection of PC, while PKC-{epsilon} translocation by PC was not interfered with 5-HD. Diazoxide, a mitoKATP opener, infused 10 min before ischemia limited infarct size to 5.2±1.4%, but this agent neither translocated PKC-{epsilon} by itself nor accelerated PKC-{epsilon} translocation after ischemia. Together with the results of earlier studies showing mitoKATP opening by PKC, the present results suggest that mitoKATP-mediated cardioprotection occurs subsequent to PKC-{epsilon} activation by PC.




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