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Originally published In Press as doi:10.1074/jbc.M101089200 on November 28, 2001

J. Biol. Chem., Vol. 277, Issue 5, 3342-3349, February 1, 2002
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Protective Roles of NF-kappa B for Chromium(VI)-induced Cytotoxicity Is Revealed by Expression of Ikappa B Kinase-beta Mutant*

Fei ChenDagger §, Jacquelyn Bower, Stephen S. Leonard, Min Ding, Yongju Lu, Yon Rojanasakul, Hsiang-fu Kung||, Val Vallyathan, Vince Castranova, and Xianglin Shi**

From the Health Effects Laboratory Division, NIOSH, Morgantown, West Virginia 26505, the  Department of Basic Pharmaceutical Sciences, West Virginia University, Morgantown, West Virginia 26506, and the || Institute of Molecular Biology, University of Hong Kong, Hong Kong, People's Republic of China

To delineate the molecular mechanisms of NF-kappa B-mediated regulation of chromium(VI)-induced cell death, the signaling pathway leading to the activation of NF-kappa B was interrupted by stable transfection of a kinase-mutated form of Ikappa B kinase beta  (IKKbeta -KM). Here we demonstrate a novel role for the NF-kappa B transcription factor in inhibiting chromium(VI)-induced cell death. Inhibition of NF-kappa B by IKKbeta -KM or IKKbeta gene deficiency resulted in a spontaneous cleavage of Bcl-xl antiapoptotic protein due to the elevated caspase-3 activity. DNA microarray assay suggested a decreased expression of genes encoding antiapoptotic proteins, cIAP1 and cIAP2, in the cells overexpressing IKKbeta -KM. Chromium(VI) treatment of these NF-kappa B-inhibited cells induced necrotic-like cell death. Such chromium(VI)-induced cell killing could be partially inhibited by expression of exogenous cIAP1, an inhibitor of caspases, indicating that caspases along with others may be involved in chromium(VI)-induced cell death. These results suggest that NF-kappa B is essential for inhibiting toxic metal-induced cytotoxicity. Such inhibition may involve up-regulation of the expression of anti-death proteins including cIAP1 that prevents spontaneous caspase activation and subsequent cleavage of Bcl-xl protein.

* This study was supported in part under the Interagency Agreement (98-18-00 m2) between the Occupational Safety and Health Administration and NIOSH.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Dagger Supported by a Career Development Award under a cooperative agreement from the Centers for Disease Control and Prevention through the Association of Teachers of Preventive Medicine.

§ To whom correspondence and reprint requests may be addressed: PPRB of NIOSH, 1095 Willowdale Rd., Morgantown, WV 26505. Tel.: 304-285-6021/6158; Fax: 304-285-5938; E-mail: lfd3@cdc.gov.

** To whom correspondence and reprint requests may be addressed: PPRB of NIOSH, 1095 Willowdale Rd., Morgantown, WV 26505. Tel.: 304-285-6021/6158; Fax: 304-285-5938; E-mail: xshi@cdc.gov.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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