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Blood, Vol. 93 No. 9 (May 1), 1999:
pp. 2928-2935
Hematopoietic Growth Factors Signal Through the Formation of
Reactive Oxygen Species
Martin Sattler,
Thomas Winkler,
Shalini Verma,
Christopher H. Byrne,
Gautam Shrikhande,
Ravi Salgia, and
James D. Griffin
From the Department of Adult Oncology, Dana-Farber Cancer Institute,
Harvard Medical School, Boston, MA.
Hematopoietic growth factors (HGFs) stimulate growth,
differentiation, and prevent apoptosis of progenitor cells. Each growth factor has a specific cell surface receptor, which activates both unique and shared signal transduction pathways. We found that several
HGFs, including granulocyte-macrophage colony-stimulating factor
(GM-CSF), interleukin-3 (IL-3), steel factor (SF), and thrombopoietin
(TPO) induce a rapid increase in reactive oxygen species (ROS) in
quiescent cells. In an effort to understand the potential biochemical
and biological consequences of increased ROS in these cells, we exposed
growth factor-deprived cells to hydrogen peroxide
(H2O2) at concentrations that increased
intracellular ROS. H2O2 induced a
dose-dependent increase in tyrosine phosphorylation, including
increased tyrosine phosphorylation of the GM-CSF receptor beta chain
( c), STAT5, and other signaling proteins.
H2O2 also induced expression of the early
response gene c-FOS, and G1- to S-phase transition, but not S- to
G2/M-phase transition of MO7e cells. The cell permeable antioxidant
pyrrolidine dithiocarbamate (PDTC) decreased the intracellular levels
of ROS and inhibited tyrosine phosphorylation induced by GM-CSF in MO7e
cells, suggesting that ROS generation plays an important role in GM-CSF
signaling. Consistent with this notion, PDTC and two other
antioxidants, N-acetyl cysteine and 2-mercaptoethanol, reduced growth
and viability of MO7e cells. These results suggest that generation of
ROS in response to HGFs may contribute to downstream signaling events, especially those involving tyrosine phosphorylation.
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