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Cardiovascular Research 2007 73(4):794-805; doi:10.1016/j.cardiores.2006.12.016
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Copyright © 2006, European Society of Cardiology

Soluble TNF receptors prevent apoptosis in infiltrating cells and promote ventricular rupture and remodeling after myocardial infarction

Yoshiya Mondena, Toru Kubotaa,*, Takaki Tsutsumia, Takahiro Inouea, Shunichi Kawanoa, Natsumi Kawamuraa, Tomomi Idea, Kensuke Egashiraa, Hiroyuki Tsutsuib and Kenji Sunagawaa

aDepartment of Cardiovascular Medicine, Kyushu University Graduate School of Medical Sciences, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan
bDepartment of Cardiovascular Medicine, Hokkaido University Graduate School of Medicine, Kita-15, Nishi-7, Kita-ku, Sapporo 060-8638, Japan

* Corresponding author. Tel.: +81 92 642 5359; fax: +81 92 642 5374. Email address: kubotat{at}cardiol.med.kyushu-u.ac.jp

Objective: Tumor necrosis factor (TNF)-{alpha} induced in damaged myocardium has been considered to be cardiotoxic. However, the negative results of RENEWAL and ATTACH prompt us to reconsider the role of TNF-{alpha} in cardiovascular diseases. The present study aimed to evaluate the effects of soluble TNF receptor treatment on myocardial infarction (MI).

Methods: An adenovirus encoding a 55-kDa TNF receptor-IgG fusion protein (AdTNFR1) was used to neutralize TNF-{alpha}, and an adenovirus encoding LacZ (AdLacZ) served as control. In the pre-MI treatment protocol, mice were given an intravenous injection of AdTNFR1 or AdLacZ 1 week before left coronary artery ligation to induce MI. In the post-MI treatment protocol, mice were treated with AdTNFR1 or AdLacZ 1 week after left coronary ligation.

Results: Treatment with AdTNFR1 neutralized bioactivity of TNF-{alpha} that was activated after MI and prevented apoptosis of infiltrating cells in infarct myocardium. However, pre-MI treatment with AdTNFR1 promoted ventricular rupture by reducing fibrosis with further activation of matrix metalloproteinase (MMP)-9. Post-MI treatment with AdTNFR1 exacerbated ventricular dysfunction and remodeling, with enhanced fibrosis of non-infarct myocardium with further MMP-2 activation.

Conclusions: Both pre- and post-MI treatments with AdTNFR1 were deleterious in a mouse MI model. Thus, TNF-{alpha} may play not only toxic but also protective roles in MI.

KEYWORDS Apoptosis; Cytokines; Infarction; Matrix metalloproteinases; Remodeling

Time for primary review 27 days


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