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Am J Physiol Cell Physiol 283: C831-C838, 2002; doi:10.1152/ajpcell.00045.2002
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Vol. 283, Issue 3, C831-C838, September 2002

Regulation of Fas (CD95)-induced apoptosis by nuclear factor-kappa B and tumor necrosis factor-alpha in macrophages

Bin Lu1, Liying Wang2, Djordje Medan1, David Toledo1, Chuanshu Huang3, Fei Chen2, Xianglin Shi2, and Yon Rojanasakul1

1 Department of Basic Pharmaceutical Sciences, Health Sciences Center, West Virginia University, Morgantown 26506; 2 Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, West Virginia 26505; and 3 Nelson Institute of Environmental Medicine, New York University, Tuxedo, New York 10016

The APO-1/Fas ligand (FasL) and tumor necrosis factor-alpha (TNF-alpha ) are two functionally related molecules that induce apoptosis of susceptible cells. Although the two molecules have been reported to induce apoptosis via distinct signaling pathways, we have shown that FasL can also upregulate the expression of TNF-alpha , raising the possibility that TNF-alpha may be involved in FasL-induced apoptosis. Because TNF-alpha gene expression is under the control of nuclear factor-kappa B (NF-kappa B), we investigated whether FasL can induce NF-kappa B activation and whether such activation plays a role in FasL-mediated cell death in macrophages. Gene transfection studies using NF-kappa B-dependent reporter plasmid showed that FasL did activate NF-kappa B promoter activity. Gel shift studies also revealed that FasL mobilized the p50/p65 heterodimeric form of NF-kappa B. Inhibition of NF-kappa B by a specific NF-kappa B inhibitor, caffeic acid phenylethyl ester, or by dominant expression of the NF-kappa B inhibitory subunit Ikappa B caused an increase in FasL-induced apoptosis and a reduction in TNF-alpha expression. However, neutralization of TNF-alpha by specific anti-TNF-alpha antibody had no effect on FasL-induced apoptosis. These results indicate that FasL-mediated cell death in macrophages is regulated through NF-kappa B and is independent of TNF-alpha activation, suggesting the antiapoptotic role of NF-kappa B and a separate death signaling pathway mediated by FasL.

tumor necrosis factor-alpha receptor; caspase-activated deoxyribonuclease


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