Abstract
See article by Ikeno et al. [1] (pages 699–709) in this issue. In the paper “Impaired perfusion after myocardial infarction is due to reperfusion-induced δPKC-mediated myocardial damage” by Ikeno et al. [1], Dr. Daria Mochly-Rosen's group at Stanford University have demonstrated a novel molecular interventional strategy, targeted inhibition of the δ isoform of protein kinase C (δPKC), to treat the post-ischemic no-reflow phenomenon in the myocardium using both mouse and pig models. This they achieved by either expressing a δPKC-specific translocation inhibitor protein fragment, δV1-1, only in cardiomyocytes in a transgenic crystalloid perfused mouse ex-vivo acute global myocardial ischemia (30 min)/reperfusion (120 min) model or through intra-coronary delivery of the TAT-conjugated synthetic peptide δV1-1 during the last minute of ischemia in a porcine in-vivo regional (LAD) myocardial ischemia (30 min)/reperfusion (30 min, 24 h, 6 and 12 days) model. Their mouse experiments showed a roughly 70% reduction in both infarction and coronary vascular resistance 5 min after reflow compared to wild-type hearts. Direct coronary delivery of the δV1-1 peptide in wild-type hearts provided similar results and, when added to the δV1-1 transgenic hearts, essentially eliminated the rise in coronary vascular resistance although no further reduction in muscle necrosis was achieved. These results suggest that δPKC inhibition protects both cardiomyocytes and microvasculature, as indicated by these investigators [1]. Their pig model included the contribution of blood cells and energy demand on the in vivo ischemic heart and involved regional ischemia more closely mimicking the clinical setting of reperfusion therapy in acute myocardial infarction. The δV1-1 peptide intra-coronary infusion performed as … *Corresponding author. Division of Cell Biology, Research Institute, The Hospital for Sick Children, Toronto, ON, Canada M5G 1X8. Tel.: +1 416 813 2095; fax: +1 416 813 5965. Email address: gregory.wilson{at}sickkids.ca
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