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This Article Full Text Full Text (PDF) All Versions of this Article: 293/4/H2219    most recent 01306.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Guo, D. Articles by Johnson, J. A. Search for Related Content PubMed PubMed Citation Articles by Guo, D. Articles by Johnson, J. A.

Protein kinase C- coimmunoprecipitates with cytochrome oxidase subunit IV and is associated with improved cytochrome-c oxidase activity and cardioprotection

¹Department of Pharmacology and Toxicology, School of Medicine, and ²The Program in Regenerative Medicine, Institute of Molecular Medicine and Genetics, Medical College of Georgia, Augusta, Georgia

Submitted 29 November 2006 ; accepted in final form 8 July 2007

We have utilized an in situ rat coronary ligation model to establish a PKC- cytochrome oxidase subunit IV (COIV) coimmunoprecipitation in myocardium exposed to ischemic preconditioning (PC). Ischemia-reperfusion (I/R) damage and PC protection were confirmed using tetrazolium-based staining methods and serum levels of cardiac troponin I. Homogenates prepared from the regions at risk (RAR) and not at risk (RNAR) for I/R injury were fractionated into cell-soluble (S), 600 g low-speed centrifugation (L), Percoll/Optiprep density gradient-purified mitochondrial (M), and 100,000 g particulate (P) fractions. COIV immunoreactivity and cytochrome-c oxidase activity measurements estimated the percentages of cellular mitochondria in S, L, M, and P fractions to be 0, 55, 29, and 16%, respectively. We observed 18, 3, and 3% of PKC-, -, and - isozymes in the M fraction under basal conditions. Following PC, we observed a 61% increase in PKC- levels in the RAR M fraction compared with the RNAR M fraction. In RAR mitochondria, we also observed a 2.8-fold increase in PKC- serine 729 phosphoimmunoreactivity (autophosphorylation), indicating the presence of activated PKC- in mitochondria following PC. PC administered before prolonged I/R induced a 1.9-fold increase in the coimmunoprecipitation of COIV, with anti-PKC- antisera and a twofold enhancement of cytochrome-c oxidase activity. Our results suggest that PKC- may interact with COIV as a component of the cardioprotection in PC. Induction of this interaction may provide a novel therapeutic target for protecting the heart from I/R damage.

cardiac; ischemia-reperfusion; protein kinase C; oxidative phosphorylation; coronary ligation; mitochondria

This article has been cited by other articles:

				Q. Yu, T. Nguyen, M. Ogbi, R. W. Caldwell, and J. A. Johnson Differential loss of cytochrome-c oxidase subunits in ischemia-reperfusion injury: exacerbation of COI subunit loss by PKC-{varepsilon} inhibition Am J Physiol Heart Circ Physiol, June 1, 2008; 294(6): H2637 - H2645. [Abstract] [Full Text] [PDF]