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J. Biol. Chem., Vol. 279, Issue 5, 3596-3604, January 30, 2004
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Preservation of Base-line Hemodynamic Function and Loss of Inducible Cardioprotection in Adult Mice Lacking Protein Kinase C
*
¶
From the
Department of Medicine and **Department of Neurology and Ernest Gallo Research Center, University of California, San Francisco, California 94110 and ||Department of Molecular Pharmacology, Stanford University, School of Medicine, Stanford, California 94305
Signaling pathways involving protein kinase C isozymes are modulators of cardiovascular development and response to injury. Protein kinase C
activation in cardiac myocytes reduces necrosis caused by coronary artery disease. However, it is unclear whether protein kinase C function is required for normal cardiac development or inducible protection against oxidative stress. Protein kinase C
activation is also observed during cardiac preconditioning. However, its role as a promoter or inhibitor of injury is controversial. We examined hearts from protein kinase C knock-out mice under physiological conditions and during acute ischemia reperfusion. Null-mutant and wild-type mice displayed equivalent base-line morphology and hemodynamic function. Targeted disruption of the protein kinase C gene blocked cardioprotection caused by ischemic preconditioning and 
1-adrenergic receptor stimulation. Protein kinase C activation increased in protein kinase C knock-out myocytes without altering resistance to injury. These observations support protein kinase C activation as an essential component of cardioprotective signaling. Our results favor protein kinase C activation as a mediator of normal growth. This study advances the understanding of cellular mechanisms responsible for preservation of myocardial integrity as potential targets for prevention and treatment of ischemic heart disease.
Received for publication, October 20, 2003
* This study was funded by National Institutes of Health Grant 5R01AA011135. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
¶ Supported by National Institutes of Health Grant 5T32GM007546 in the Division of Clinical Pharmacology at University of California San Francisco and by an Austrian Federal Fellowship for Young Investigators.
To whom correspondence should be addressed: Division of Cardiology 5G1, San Francisco General Hospital, 1001 Potrero Ave., San Francisco, CA 94110. Tel.: 415-206-8613; Fax: 415-206-5100; E-mail: gray{at}medicine.ucsf.edu.
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