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Am J Physiol Heart Circ Physiol 279: H492-H501, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 2, H492-H501, August 2000

PKC-dependent delayed metabolic preconditioning is independent of transient MAPK activation

James W. Mockridge1, Anu Punn1, David S. Latchman2, Michael S. Marber1, and Richard J. Heads1

1 Department of Cardiology, King's College London, The Rayne Institute, St. Thomas' Hospital, London, SE1 7EH; and 2 Institute of Child Health, London, WC1N 1EH, United Kingdom

In this study we used an in vitro model of delayed preconditioning to investigate activation of mitogen-activated protein kinases (MAPKs) and their potential role in protection. Neonatal rat cardiomyocytes were preconditioned using a buffer containing glycolytic inhibitors and low pH (minimal metabolic preconditioning; MMPC) consisting of modified Krebs buffer, 10 mM 2-deoxyglucose, and 20 mM lactate, pH 6.8, for 2 h followed by 24 h of simulated reperfusion before lethal simulated ischemia (LSI). MAPK activation during the MMPC protocol was determined using phospho-specific antisera and the effect on protection determined following LSI. Rapid, transient phosphorylation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) and p38 MAPK was observed during each of the MMPC, reperfusion, and LSI phases; an effect blocked by MAPK inhibitors PD-98059 and SB-203580, respectively, but not by the protein kinase C (PKC) inhibitor Ro31-8220. However, although MMPC was blocked by Ro31-8220, treatment with the MAPK inhibitors during the preconditioning protocol did not block delayed protection conferred by MMPC. Thus the data suggest that, in this model of delayed preconditioning, protection appears to be PKC dependent but independent of ERK1/2 or p38 MAPK activation.

cytoprotection; mitogen-activated protein kinases; extracellular signal-regulated kinases; p38; protein kinase C; cardiomyocytes


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