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Does Not Play a Requisite Role in Old Rabbits
1 Department of Emergency Medicine and Anesthesiology, University of Massachusetts Medical School, Worcester, MA, USA; Heart Institute, Good Samaritan Hospital, Los Angeles, CA, USA; Department of Medicine, Section of Cardiology, University of Southern California, Los Angeles, CA, USA
2 Heart Institute, Good Samaritan Hospital, Los Angeles, CA, USA
3 Heart Institute, Good Samaritan Hospital, Los Angeles, CA, USA; Department of Medicine, Section of Cardiology, University of Southern California, Los Angeles, CA, USA
* To whom correspondence should be addressed. E-mail: Karin.Przyklenk{at}umassmed.edu.
Data obtained from adult cohorts has implicated activation/translocation of protein kinase C (PKC)-
as an important cellular mediator of myocardial infarct size reduction with ischemic preconditioning (PC). Age-related alterations in cellular signaling may, however, confound the extrapolation of mechanistic insight derived from adults to the aging population -- the specific subset in which cardioprotection is undoubtedly most relevant. Accordingly, our aim was to investigate the role of PKC as a mediator of infarct size reduction with preconditioning in old versus adult rabbits. In Protocol 1, we assessed the effect of PKC translocation inhibitor peptide (PKC-TIP) and the pan-PKC inhibitor chelerythrine on infarct size reduction with PC in adult and ~4 year old rabbits, a population previously shown to exhibit definitive hallmarks of cardiovascular aging. Rabbits received 5 min of PC ischemia or a matched control period followed by 30 min of coronary artery occlusion and 3 h of reperfusion, with infarct size (delineated by tetrazolium staining) serving as the primary endpoint. In Protocol 2, we obtained preliminary insight (by Western immunoblotting) into the subcellular redistribution of PKC in response to the 5 min PC stimulus in adult and old rabbits. In adults, infarct size reduction with PC was abrogated by both PKC-TIP and chelerythrine. However, in old rabbits: (i) PC-induced cardioprotection was maintained despite inhibitor treatment; and (ii) brief PC ischemia was not associated with activation/translocation of PKC. Thus, the mechanisms responsible for PC are age-related in rabbit heart, with no apparent, requisite role of PKC in aging animals.
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