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Articles in PresS, published online ahead of print November 7, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00851.2002
Submitted on September 23, 2002
Accepted on November 4, 2002
B Induced During Myocardial Reperfusion and Reduces Reperfusion Injury
1 Department of Medicine, University of North Carolina, Chapel Hill, NC, USA
2 Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, NC, USA
3 Division of Laboratory Animal Medicine, University of North Carolina, Chapel Hill, NC, USA
4 Lineberger Comprehensive Cancer Center, Department of Biology and Curriculum in Genetics and Molecular Biology, University of North Carolina, Chapel Hill, NC, USA
5 Millenium Pharmaceuticals, Cambridge, MA, USA
6 Department of Medicine, University of North Carolina, Chapel Hill, NC, USA; Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, NC, USA
* To whom correspondence should be addressed. E-mail: tnichols{at}med.unc.edu.
Both acute coronary occlusion and reperfusion of an infarct-related artery lead to significant myocardial cell death. Recent evidence has been presented that activation of the transcription factor nuclear factor-kappa B (NF-
B) plays a critical role in reperfusion injury. NF-B is usually bound to its inhibitor, IB, and classic activation of NF-B occurs when the 20S proteasome degrades IB that has been phosphorylated and ubiquitinated. In this study, activation of NF-B was inhibited by systemic administration of a 20S proteasome inhibitor (PS-519) in a porcine model of myocardial reperfusion injury. The experimental protocol induced myocardial ischemia in the distribution of the left anterior descending coronary artery for one hour with subsequent reperfusion for three hours. A single systemic treatment with PS-519 reduced 20S proteasome activity, blocked activation of NF-B induced by reperfusion, inhibited creatine kinase, creatine kinase MB and troponin I release from the myocardium, preserved regional myocardial function measured by segmental shortening, significantly reduced the size of myocardial infarction and exhibited no acute toxicity. These data show that myocardial reperfusion injury can be inhibited by using proteasome inhibitors which likely function through the inhibition of NF-B activation.
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