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Blood, 15 December 2000, Vol. 96, No. 13, pp. 4204-4211
HEMATOPOIESIS
Interferon- -induced apoptotic responses of Fanconi anemia
group C hematopoietic progenitor cells involve caspase 8-dependent
activation of caspase 3 family members
R. Keaney Rathbun,
Tracy A. Christianson,
Gregory R. Faulkner,
Gary Jones,
Winifred Keeble,
Michael O'Dwyer, and
Grover C. Bagby
From the Division of Hematology and Medical Oncology,
Oregon Health Sciences University, Portland, OR, and the Molecular
Hematopoiesis Laboratory, NW VA Cancer Research Center, Portland, OR.
Hematopoietic progenitor cells (HPC) from mice nullizygous at the
Fanconi anemia (FA) group C locus and children with Fanconi anemia
group C (FA-C) are hypersensitive to interferon-gamma (IFN- ) and
tumor necrosis factor- . This hypersensitivity results, in part, from
the capacity of these cytokines to prime the fas pathway. Because fas-mediated programmed cell death in many cells
involves sequential activation of specific caspases, we tested the
hypothesis that programmed cell death in FA HPC involves the ordered
activation of specific caspase molecules. Lysates from lymphoblasts
treated with both agonistic anti-fas antibody and IFN-
contained activated caspase 3 family members (caspases 3, 6, and 7), as
well as caspase 8, whereas activation of caspases 1, 2, 4, 9, and 10 was not detected. The apoptotic effects of fas agonists in
IFN--treated human and murine FA-C cells were blocked when
pretreated with inhibitors (ac-DEVD-cho, CP-DEVD-cho, Z-DEVD-FMK) of
the caspase 3 protease. Inhibitors (ac-YVAD-cho, CP-YVAD-cho,
Z-YVAD-FMK) of caspase 1 did not block apoptosis or caspase 3 activation. Treatment of FA cells with the fluoromethyl ketone
tetrapeptide caspase 8 inhibitor (ac-IETD-FMK) did suppress caspase 3 activation. A 4-fold greater fraction of IFN-induced FA-C cells
expressed caspase 3 than FA-C cells complemented by retroviral-mediated
transfer of FANCC. Therefore fas-induced apoptosis in
Fanconi anemia cells of the C type involves the activation of caspase
8, which controls activation of caspase 3 family members and one direct
or indirect function of the FANCC protein is to suppress apoptotic
responses to IFN- upstream of caspase 3 activation.
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