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Vol. 62, Issue 2, 313-319, August 2002
Departments of Pathobiological Sciences (T.J.P., S.O., C.J.C.) and
Pharmacology (C.R.J.), and The Environmental Health Sciences Center for
Developmental and Molecular Toxicology (T.J.P., S.O., C.R.J., C.J.C.),
University of Wisconsin, Madison, Wisconsin
Polycyclic aromatic hydrocarbons (PAHs) have been demonstrated to cause
a variety of tumors and immunosuppressive effects. Our laboratory, and
others, have demonstrated that coculture of progenitor B lymphocytes
(pre-B cells) with bone marrow stromal cells and the model PAH
7,12-dimethylbenz[a]anthracene (DMBA) results in pre-B
cell apoptosis. In this study we investigated the molecular events that
precede apoptosis in DMBA-treated 70Z/3 cells, a pre-B cell line. Using
caspase activity assays and immunoblotting techniques, we determined
the temporal pattern of caspase expression in the pre-B cells. Using
caspase inhibitors, we demonstrated that DMBA-mediated pre-B cell
apoptosis is dependent on activation of caspase-8, whereas caspase-9
activation is essential for maximal apoptosis. We also demonstrated
that DMBA activated PKR, an interferon-inducible protein kinase, in
pre-B cells. PKR in turn can activate caspase-8 independently of death
receptor ligation. As a result of these studies, we propose a novel
PKR-dependent pathway for activation of apoptosis in DMBA-treated pre-B cells.
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