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Circulation Journal
Vol. 70 (2006) No. 12 p. 1635-1642

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http://doi.org/10.1253/circj.70.1635

Experimental Investigation

Background Tumor necrosis factor (TNF)-α is linked to the pathogenesis of cardiovascular diseases, but how it affects myocardial infarction (MI), so the present study examined the effects of TNF-α and the involvement of intercellular adhesion molecule (ICAM)-1 on MI. Methods and Results Left coronary arteries of C57BL/6 wild type (WT) and TNF-α knockout (KO) mice were ligated and the mice were killed 1, 3, and 7 days later. Fractional shortening on echocardiography of the KO mice was significantly higher than that of the WT mice from day 1 to 7 (p<0.01). The ICAM-1 mRNA in the infarcted area of the KO mice was significantly lower than that of the WT from day 1 (p<0.01) to 7. In immunohistochemistry, the expression of ICAM-1 was weaker in the KO than in the WT mice. The number of neutrophils in the KO mice peaked at day 1, but even this peak level failed to reach the levels in the infarcted (p<0.01) and peri-infarcted areas (p<0.05) in the WT. The number of macrophages in the KO mice peaked at day 7, but this peak level failed to reach the levels in the infarcted (p<0.01) and peri-infarcted areas (p<0.05) in the WT. Conclusion In a permanent occlusion model of MI TNF-α decreased cardiac function and ameliorated myocardial remodeling through the induction of ICAM-1. (Circ J 2006; 70: 1635 - 1642)

Copyright © 2006 THE JAPANESE CIRCULATION SOCIETY

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