Hepatocyte FADD/MORT1 levels increase in response to pro-apoptotic stimuli

doi:10.1074/jbc.M203484200

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Papers In Press, published online ahead of print August 6, 2002
J. Biol. Chem, 10.1074/jbc.M203484200
Submitted on April 10, 2002
Revised on July 29, 2002
Accepted on August 5, 2002

Hepatocyte FADD/MORT1 levels increase in response to pro-apoptotic stimuli

Peter K.M. Kim, Yinna Wang, Andrea Gambotto, Young-Myeong Kim, Richard Weller, Brian S. Zuckerbraun, Yun Hua, Simon C. Watkins, and Timothy R. Billiar

Department of Surgery, University of Pittsburgh Medical School, Pittsburgh, PA 15213

Corresponding Author: kimp{at}msx.upmc.edu

We examined the regulation of FADD protein as an important adaptor molecule in apoptosis signaling and hypothesized that the regulation of FADD could contribute to hepatocyte death. FADD/MORT1 is required for activation of several signaling pathways of cell death. In this study we report the interesting and unexpected result that actinomycin D increased the expression of FADD protein, and we demonstrate that other cellular stresses like ultraviolet irradiation or heat shock could also increase FADD levels in hepatocytes. In cells treated with actinomycin D, FADD levels were elevated homogeneously in the cytoplasm. The increase in cytoplasmic FADD protein by actinomycin D or FADD overexpression alone both correlated with cell death, and specific anti-sense inhibition of FADD expression consistently diminished approximately 30% of the cell death induced by actinomycin D. These data indicate that FADD protein expression can increase rapidly in hepatocytes exposed to broadly cytotoxic agents.

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