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Am J Physiol Heart Circ Physiol (April 21, 2006). doi:10.1152/ajpheart.01175.2005
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Submitted on November 6, 2005
Accepted on April 12, 2006

Blockade of NF-&kgr;B improves cardiac function and survival after myocardial infarction

Shunichi Kawano1, Toru Kubota1*, Yoshiya Monden1, Takaki Tsutsumi1, Takahiro Inoue1, Natsumi Kawamura1, Hiroyuki Tsutsui2, and Kenji Sunagawa1

1 Kyushu University Graduate School of Medical Sciences, Department of Cardiovascular Medicine, Fukuoka, Japan
2 Hokkaido University Graduate School of Medicine, Department of Cardiovascular Medicine, Sapporo, Japan

* To whom correspondence should be addressed. E-mail: kubotat{at}cardiol.med.kyushu-u.ac.jp.

NF-{kappa}B is a key transcription factor that regulates inflammatory processes. In the present study, we tested the hypothesis that blockade of NF-{kappa}B ameliorate cardiac remodeling and failure after myocardial infarction (MI). Knock-out mice with targeted disruption of the p50 subunit of NF-{kappa}B (KO) were used to block the activation of NF-{kappa}B. MI was induced by ligation of the left coronary artery in male KO and age-matched wild-type (WT) mice. NF-{kappa}B was activated in non-infarct as well as infarct myocardium in WT+MI mice, while the activity was completely abolished in KO mice. Blockade of NF-{kappa}B significantly reduced early ventricular rupture after MI and improved the survival by ameliorating congestive heart failure. Echocardiographic and pressure measurement revealed that left ventricular fractional shortening and + dP/dtmax were significantly increased and end-diastolic pressure was significantly decreased in KO+MI mice compared to WT+MI mice. Histological analysis demonstrated significant suppression of myocyte hypertrophy as well as interstitial fibrosis in non-infarct myocardium in KO+MI mice. Blockade of NF-{kappa}B did not ameliorate expression of proinflammatory cytokines in infarct or non-infarct myocardium. In contrast, phosphorylation of c-Jun N-terminal kinase was almost completely abolished in KO+MI mice. The present study demonstrates that targeted disruption of the p50 subunit of NF-{kappa}B reduces ventricular rupture as well as improves cardiac function and survival after MI. Blockade of NF-{kappa}B might be a new therapeutic strategy to attenuate cardiac remodeling and failure after MI.




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