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Am J Physiol Gastrointest Liver Physiol (January 16, 2002). doi:10.1152/ajpgi.00467.2001
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Articles in PresS, published online ahead of print January 16, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00467.2001
Submitted on November 1, 2001
Accepted on January 9, 2002

Novel Effects of Staurosporine on Mouse Hepatocytes: Cytochrome c Independent Apoptosis and Inhibition of NF-{kappa}B Transactivation

Guoping Feng1 and Neil Kaplowitz1*

1 Medicine, University of Southern California Keck School of Medicine, Los Angeles, CA, none

* To whom correspondence should be addressed. E-mail: kaplowit{at}hsc.usc.edu.

Staurosporine (STS) induces apoptosis in various cell lines. We report in this study that primary cultured mouse hepatocytes are less sensitive to STS compared with Jurkat cells and Huh-7 cells. In contrast to the cell lines, no apparent release of cytochrome c or loss of mitochondrial transmembrane potential was detected in primary hepatocytes undergoing STS-induced apoptosis. Caspase-3 was activated in primary hepatocytes by STS treatment, but caspase-9 and caspase-12 were not activated and caspase-3 activation is not dependent on caspase-8. These findings point to a novel pathway for caspase-3 activation by STS in primary hepatocytes. Pretreatment with caspase inhibitor converted STS-induced apoptosis of hepatocytes to necrotic cell death without significantly changing total cell death. Thus, STS causes hepatocytes to commit to death upstream of the activation of caspases. We also demonstrated that STS dramatically sensitized primary hepatocytes to TNF- {alpha} induced apoptosis. STS activated I{kappa}B kinase and NF-{kappa}B nuclear translocation and DNA binding but inhibited transactivation of I{kappa}B-{alpha}, iNOS, and IAP-1 in hepatocytes and NF-{kappa}B reporter in transfected Huh-7 cells.




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