AJP - Heart and Circulatory Physiology, Vol 270, Issue 4 1231-H1239, Copyright © 1996 by American Physiological Society

ARTICLES

Tumor necrosis factor-alpha-induced expression of heat shock protein 72 in adult feline cardiac myocytes

M. Nakano, A. A. Knowlton, T. Yokoyama, W. Lesslauer and D. L. Mann
Department of Medicine, Veterans Affairs Medical Center, Houston, Texas, USA.

Tumor necrosis factor-alpha (TNF-alpha) is a proinflammatory cytokine that is elaborated in a myriad of cardiac disease states. Although the biological role for TNF-alpha in the adult heart is not known, a recent study in fetal myocardial cells has shown that this cytokine increases the synthesis of low-molecular-weight stress proteins. These findings suggested the interesting possibility that TNF-alpha might play a functional role in the adult heart by increasing the expression of stress proteins in cardiac myocytes. Accordingly, the purpose of this study was to determine whether TNF-alpha would modulate the expression of heat shock protein 72 (HSP 72), a stress protein that is thought to exert protective effects in the adult heart. Stimulation of adult feline cardiac myocytes with a range of TNF-alpha concentrations (10-1,000 U/ml) for 12 h showed that concentrations of TNF-alpha < or = 10 U/ml had no effect on HSP 72 expression: increased HSP 72 expression was detected 3 h following cytokine stimulation, peaked by approximately 12 h, and then returned toward baseline by 48 h. Additional studies indicated that stimulation of the type 1 TNF receptor was responsible for the increase in HSP 72 expression. In summary, these studies constitute the initial demonstration that TNF-alpha exerts concentration- and time-dependent effects on the expression of HSP 72 in the adult mammalian cardiac myocytes, thus suggesting the interesting possibility that the elaboration of TNF-alpha may enable the heart to better withstand certain forms of stress.

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