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Am J Physiol Heart Circ Physiol 280: H1464-H1471, 2001;
0363-6135/01 $5.00
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Vol. 280, Issue 4, H1464-H1471, April 2001

Targeted disruption of ICAM-1, P-selectin genes improves cardiac function and survival in TNF-alpha transgenic mice

Ana Lia Graciano1, Debora D. Bryant1, D. Jean White2, Jureta Horton2, Neil E. Bowles3, and Brett P. Giroir1

1 Crystal Charity Ball Center for Pediatric Critical Care Research and Division of Critical Care, Department of Pediatrics, and 2 Department of Surgery, University of Texas Southwestern Medical Center at Dallas, Dallas 75390-9063; and 3 Department of Pediatrics, Baylor College of Medicine, Houston, Texas 77030

We have developed a transgenic mouse model in which tumor necrosis factor (TNF)-alpha is overexpressed exclusively in the heart under the regulation of the alpha -myosin heavy chain promoter. These animals develop chronic heart failure associated with severe leukocyte infiltration in both the atria and the ventricles. The purpose of this study was to investigate the role of adhesion molecules in mediating cardiac dysfunction in the TNF-alpha transgenic model. TNF-alpha transgenic mice were bred with mice null for intercellular adhesion molecule (ICAM)-1 and P-selectin genes to obtain a lineage of ICAM-1 and P-selectin null mice with selective overexpression of TNF-alpha in the heart. TNF-alpha transgenic animals showed marked upregulation of ICAM-1 mRNA and protein; however, P-selectin mRNA and protein remained undetectable despite chronic TNF overexpression. Cardiac function was markedly improved in the ICAM-1-/-, P-selectin-/-, TNF-alpha transgenic group versus the ICAM+/+, P-selectin+/+, TNF-alpha transgenic group. Kaplan-Meier survival curves showed statistically significant prolonged survival in the ICAM-1-/-, P-selectin-/-, TNF-alpha transgenic animals. These data suggest that ICAM-1 mediates at least in part the cardiac dysfunction induced by TNF-alpha expression by cardiac myocytes.

sepsis; congestive heart failure; cytokines; endotoxin


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