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Articles in PresS, published online ahead of print June 13, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.01089.2001
Submitted on December 12, 2001
Accepted on June 10, 2002
1 Hatter Institute for Cardiovascular Studies, University College London Hospital and Medical School, London, United Kingdom; The Institute of Child Health, University College London, London, United Kingdom
2 The Institute of Child Health, University College London, London, United Kingdom
3 Hatter Institute for Cardiovascular Studies, University College London Hospital and Medical School, London, United Kingdom
* To whom correspondence should be addressed. E-mail: hatter-institute{at}ucl.ac.uk.
Objective: Reperfusion of ischemic myocardium is essential for tissue salvage but paradoxically contributes to cell death. We hypothesized that activation of potential survival pathways such as the p42/p44 mitogen activated protein kinase (MAPK) may prevent lethal reperfusion injury. Urocortin is a peptide factor that affects the p42/p44 MAPK signaling pathway. Both isolated and in vivo rat heart models were used to examine the potential for urocortin to prevent reperfusion injury. Methods: Isolated rat hearts underwent 35min regional ischemia and 2hr reperfusion, with urocortin perfused for 20min from the onset of reperfusion. In the in vivo study, urocortin was administered as an i.v. bolus 3min prior to reperfusion, using a protocol of 25min regional ischemia and 2hr reperfusion. Blockade of the p42/p44 MAPK pathway with the inhibitor PD98059 was used in both models. Results: Urocortin attenuated lethal reperfusion-induced injury both in vitro and in vivo via a p42/p44 MAPK dependent mechanism. Furthermore, Western blot analysis demonstrated the ability of urocortin to directly upregulate this signaling pathway. Conclusion: We believe that the p42/p44 MAPK dependent signaling pathway represents an important survival mechanism against reperfusion injury.
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