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Cardiovascular Research 2007 76(3):465-472; doi:10.1016/j.cardiores.2007.08.001
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Copyright © 2007, European Society of Cardiology

The relationship between p38 mitogen-activated protein kinase and AMP-activated protein kinase during myocardial ischemia

Sebastien Jacqueta, Elham Zarrinpashnehb, Audrey Chaveyc, Audrey Ginionb, Isabelle Leclercc, Benoit Violletd, Guy A. Rutterc, Luc Bertrandb and Michael S. Marbera,*

aCardiovascular Division, King's College London, St. Thomas' Hospital, London SEI 7EH, UK
bDivision of Cardiology, School of Medicine, Université Catholique de Louvain, Brussels, Belgium
cDepartment of Cell Biology, Division of Medicine, Imperial College, London SW7 2AZ, UK
dInstitut Cochin, Université Paris Descartes, CNRS (UMR 8104) and Inserm, U567, Paris, France

*Corresponding author. Department of Cardiology, The Rayne Institute, St Thomas' Hospital, London SE1 7EH, UK. Tel.: +44 20 7188 1008; fax: +44 20 7188 0970. michael.marber{at}kcl.ac.uk

Objective p38 mitogen-activated protein kinase (p38 MAPK) and AMP-activated protein kinase (AMPK) are activated by, and influence sensitivity to, myocardial ischemia. Recently a number of studies have suggested that AMPK may participate in the activation of p38 MAPK. We therefore examined whether AMPK may be the principal "ischemia sensor" responsible for p38 MAPK activation during myocardial ischemia.

Methods We used a variety of approaches to alter AMPK activity during ischemia and studied the repercussions on p38 MAPK activation.

Results The activities of AMPK and p38 MAPK were temporally related in adult rat ventricular myocytes (ARVM) subjected to simulated ischemia and in isolated mouse hearts subjected to no-flow ischemia. However p38 MAPK activation was unaltered in mouse hearts lacking the predominant or minor myocardial isoforms, AMPK{alpha}2 or AMPK{alpha}1 respectively. Likewise, in ARVM, adenoviral-driven expression of the minor myocardial isoform AMPK{alpha}1, in a constitutively active or dominant negative form reducing AMPK activity, did not alter p38 MAPK activation under basal conditions or during simulated ischemia. Finally, pharmacological inhibition of AMPK during ischemia with compound C did not attenuate the coincident activation of p38 MAPK.

Conclusions Although AMPK and p38 MAPK are both activated during myocardial ischemia, the activation of p38 MAPK occurs independently of AMPK.

KEYWORDS Ischemia; Heart; p38-MAPK; AMPK


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