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Multiple Inhibitory Cytokines Induce Deregulated Progenitor
Growth and Apoptosis in Hematopoietic Cells From
Fac / Mice
Laura S. Haneline,
Hal E. Broxmeyer,
Scott Cooper,
Giao Hangoc,
Madeleine Carreau,
Manuel Buchwald, and
D. Wade Clapp
From the Department of Pediatrics, Herman B Wells Center for
Pediatric Research, Indiana University School of Medicine; the
Department of Microbiology/Immunology, Indiana University School of
Medicine; Walther Oncology Center, Indiana University School of
Medicine, Indianapolis; Walther Cancer Institute, Indianapolis, IN; the
Department of Genetics, Hospital for Sick Children, Toronto, Ontario,
Canada; and the Department of Molecular and Medical Genetics,
University of Toronto, Toronto, Ontario, Canada.
We used a murine model containing a disruption of the murine
homologue (Fac) of Fanconi Anemia group C (FAC)
to evaluate the role of Fac in the pathogenesis of bone marrow
(BM) failure. Methylcellulose cultures of BM cells from
Fac / and Fac+/+ mice
were established to examine the growth of multipotent and lineage-restricted progenitors containing inhibitory cytokines, including interferon- (IFN-), tumor necrosis factor-
(TNF-), and macrophage inflammatory protein-1 (MIP-1).
Clonogenic growth of Fac/ progenitors was
reduced by 50% at 50- to 100-fold lower concentrations of all
inhibitory cytokines evaluated. We hypothesized that the aberrant
responsiveness to inhibitory cytokines in clonogenic cells may be a
result of deregulated apoptosis. To test this hypothesis, we performed
the TUNEL assay on purified populations of primary BM cells enriched
for hematopoietic progenitors or differentiated myeloid cells. After
stimulation with TNF-, accentuated apoptosis was observed in both
populations of Fac/ cells. In addition,
deregulated apoptosis was also noted in the most immature phenotypic
population of hematopoietic cells after stimulation with
MIP-1.Together these data suggest a role of Fac in affecting
the signaling of multiple cytokine pathways and support
cytokine-mediated apoptosis as a major mechanism responsible for BM
failure observed in FA patients.
Blood, Vol. 91 No. 11 (June 1), 1998:
pp. 4092-4098
© 1998 by The American Society of Hematology.
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