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Am J Physiol Heart Circ Physiol (February 1, 2008). doi:10.1152/ajpheart.01346.2007
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Submitted on November 16, 2007
Accepted on January 28, 2008

PKC{beta} Modulates Ischemia Reperfusion Injury in the Heart

Linghua Kong1, Martin Andrassy1, Jong Sun Chang1, Chun Huang2, Tomohiro Asai2, Matthias J Szabolcs3, Shunichi Homma4, Rui Liu4, Yu Shan Zou1, Michael Leitges5, Shi Du Yan1, Ravichandran Ramasamy1, Ann Marie Schmidt1, and Shi-Fang Yan1*

1 Surgery, Columbia University Medical Center, New York, New York, United States
2 Surgery, Columbia University, New York, New York, United States
3 Pathology, Columbia University Medical Center, New York, New York, United States
4 Medicine, Columbia University Medical Center, United States
5 Nephrology, Hannover Medical School, Hannover, Germany

* To whom correspondence should be addressed. E-mail: sy18{at}columbia.edu.

Protein kinase C {beta}II (PKC{beta}II) is an important modulator of cellular stress responses. To test the hypothesis that PKC{beta}II modulates the response to myocardial ischemia/reperfusion (I/R) injury, we performed occlusion and reperfusion of the left anterior descending coronary artery (LAD) in mice. Homozygous PKC{beta} null (-/-) or wild type mice fed the PKC{beta} inhibitor, ruboxistaurin, displayed significantly decreased infarct size and enhanced recovery of left ventricular function; and reduced markers of cellular necrosis, serum CPK and LDH levels, compared to wild-type or vehicle-treated animals after 30 minutes of ischemia followed by 48 hours of reperfusion. Our studies revealed that membrane translocation of the PKC{beta}II isoform in left ventricule tissue was sustained after I/R and that gene deletion or pharmacological blockade of PKC{beta} protected ischemic myocardium. Homozygous deletion of PKC{beta} significantly diminished phosphorylation of c-Jun NH2-terminal mitogen activated protein kinase (JNK MAPK) and expression of activated caspase 3 in left ventricle tissue of mice subjected to I/R. These data implicate PKC{beta} in I/R-mediated myocardial injury, at least in part via phosphorylation of JNK, and suggest that blockade of PKC{beta} may represent a potent strategy to protect the vulnerable myocardium.




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