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Cardiovascular Research Advance Access [Accepted Manuscript] published online on December 20, 2007
Cardiovascular Research, doi:10.1093/cvr/cvm113
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Remote versus ischemic preconditioning: the differential role of MAP kinase pathways

Marc Heidbreder, Annegret Naumann, Klaus Tempel, Peter Dominiak and Andreas Dendorfer

Institute of experimental and clinical Pharmacology and Toxicology University Hospital Schleswig-Holstein, Campus Luebeck, Germany

Correspondence: Marc Heidbreder, M.D. Institute of experimental and clinical Pharmacology and Toxicology University Hospital Schleswig-Holstein, Campus Luebeck, Germany Ratzeburger Allee 160 23538 Luebeck, Germany Telephone: (49) (451) 500 2696 Fax: (49) (451) 500 3327 e-mail: heidbred{at}medinf.mu-luebeck.de

Aim: Since mitogen-activated protein kinases (MAPK) were found to be implicated in the signalling of ischemic preconditioning (IPC), we tested the hypothesis of a contribution of these protein kinases to remote preconditioning (RPC).

Methods: To determine the role of p38, ERK1/2 and JNK1/2 MAPK in mediating cardiac protection, an in vivo model of myocardial infarction was applied in male Wistar rats. RPC or IPC were induced by occlusion of the superior mesenteric artery or the left coronary artery, respectively. Infarct size was determined based on 2,3,5-triphenyltetrazolium chloride staining. Phosphorylation of the various MAPKs was analyzed by immunoblotting in samples of the small intestine and myocardium obtained after IPC or RPC procedures. The MAPK inhibitors SB203580 (p38), PD98059 (ERK1/2), and SP600125 (JNK1/2) were administered to assess the potential significance of MAPK signalling in RPC.

Results: Both preconditioning stimuli decreased myocardial infarct size significantly after a lethal period of ischemia. Each of the applied MAPK inhibitors was capable of abrogating the RPC-induced cardioprotection. Western blot analysis of myocardial samples revealed an increase in phosphorylated amounts of ERK1/2 and JNK1 after IPC, whereas phosphorylation of p38 protein was decreased significantly. Likewise, RPC resulted in a considerable increase in phosphorylation of ERK1/2 and JNK1/2 proteins in the small intestine, whereas it did not alter the MAPK phosphorylation state in the myocardium.

Conclusions: All investigated MAPK pathways appear to be involved in RPC-induced cardioprotection; however, they do not contribute to the alterations that define the preconditioned state of the myocardium prior to the infarction.

Time for primary review: 22


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