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Cardiovascular Research 2007 74(3):466-470; doi:10.1016/j.cardiores.2007.02.027
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Copyright © 2007, European Society of Cardiology

Post-infarction remodeling is independent of mitogen-activated protein kinase kinase 3 (MKK3)

James E. Clarka, Richard A. Flavellb, Matthew E. Fairclotha, Roger J. Davisc, Richard J. Headsa and Michael S. Marbera,*

aThe Cardiovascular Division, Kings College London, The Rayne Institute, St Thomas' Hospital, London, UK
bSection of Immunobiology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT, USA
cHoward Hughes Medical Institute, University of Massachusetts, Worcester, MA, USA

* Corresponding author. Tel.: +44 20 7188 1008; fax: +44 20 7188 0970. Email address: mike.marber{at}kcl.ac.uk

Objectives:: Our aim was to examine the role of mitogen-activated protein kinase kinase 3 (MKK3) in the development of left ventricular (LV) remodeling following myocardial infarction (MI).

Methods:: MKK3-null mice were subjected to permanent coronary artery ligation. Twenty-eight days after MI, haemodynamics in male mkk3+/+(WT) and mkk3–/–(KO) littermates were assessed using a pressure-conductance catheter. MI groups were compared to un-operated time-matched WT and KO controls.

Results:: MI caused significant LV contractile dysfunction and dilatation which did not differ by genotype. Detailed morphometric analysis of excised hearts confirmed these similar global indices of remodeling and also demonstrated that pathological changes within remote myocardium and scar did not differ between KO and WT hearts.

Conclusions:: Despite numerous lines of evidence suggesting MKK3 is the relevant kinase upstream of p38 mitogen-activated protein kinase in LV remodeling these processes can continue in its absence.

KEYWORDS Infarction; Remodeling; MKK3; p38-MAPK; Haemodynamics

Time for primary review 11 days


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