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Comparison of tumor necrosis factor-effect on the expression of iNOS in macrophage and cardiac myocytes

Circulatory Sciences Graduate Perfusion Program, Sarver Heart Center, University of Arizona, Tucson, Arizona

Douglas F Larson

Circulatory Sciences Graduate Perfusion Program, Sarver Heart Center, University of Arizona, Tucson, Arizona

Kyler Hunter

Circulatory Sciences Graduate Perfusion Program, Sarver Heart Center, University of Arizona, Tucson, Arizona

Mark Gorman

Circulatory Sciences Graduate Perfusion Program, Sarver Heart Center, University of Arizona, Tucson, Arizona

Bo Yang

Circulatory Sciences Graduate Perfusion Program, Sarver Heart Center, University of Arizona, Tucson, Arizona

Proinflammatory cytokines, including tumor necrosis factor- (TNF-), are elevated during cardiopulmonary bypass (CPB), heart failure, and inflammatory cardiac and systemic diseases. Elevated TNF- has been linked to diminished cardiac function, decreased systemic vascular resistance, as well as renal and pulmonary dysfunction. It is understood that myocardial tissues can express TNF-, which results in the induction of inducible nitric oxide synthase (iNOS) leading to a significant decline in cardiac function and other direct effects. The hypothesis of this study was to determine if TNF- would stimulate iNOS and its product nitric oxide (NO) similarly in immortalized macrophage and cardiac myocytes. Cultured macrophages (RAW 264.7) and cardiac myocytes (HL-1) were placed into two treatment groups and a control. The treatments included: (1) TNF- and lipopolysaccharide (LPS); and (2) LPS, TNF-, interleukin-1ß (IL-1ß) and interferon- (IFN-) incubated for 8 h. The macrophage expression of iNOS increased by 365% (p < 0.01) and its product, NO, increased proportionally. The expression of iNOS in the cardiac myocyte did not increase with TNF- and LPS. However, with the addition of IFN- and IL-1ß iNOS increased to 140% of control (p < 0.05). Myocyte cGMP and NO did not increase significantly with TNF- treatment. This study suggests that HL-1 myocyte iNOS cannot be induced by TNF-, unlike macrophage iNOS. Furthermore, the resultant cardiac dysfunction, secondary to proinflammatory cytokines effects, is regulated via diverse pathways.

Perfusion, Vol. 16, No. 1, 67-74 (2001)
DOI: 10.1177/026765910101600110


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