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Granulocyte colony-stimulating factor activation of Stat3 alpha and Stat3
beta in immature normal and leukemic human myeloid cells
A Chakraborty, SM White, TS Schaefer, ED Ball, KF Dyer and DJ Tweardy
Department of Medicine, University of Pittsburgh School of Medicine, PA,
USA.
Granulocyte colony-stimulating factor (G-CSF) is the cytokine critical for
directing neutrophilic granulocyte differentiation. Acute myelogenous
leukemia (AML) cells, which frequently arise from this lineage, respond
aberrantly to G-CSF by proliferating without differentiating. The basis for
this abnormal responses is unknown. In the present study, we investigated
whether G-CSF signaling in immature normal and leukemic human myeloid cells
diverges at the level of activation of signal transducers and activators of
transcription (STAT) proteins. We compared the profile of STAT proteins
activated in G-CSF- stimulated immature normal and leukemic human myeloid
cells. G-CSF activated Stat3 alpha in all AML cell lines examined except
HL60 and in three of six uncultured AML patient samples. In normal human
CD34+ bone marrow cells and HL60 cells, both reported to differentiate in
response to G-CSF, G-CSF did not activate Stat3 alpha; rather, it activated
only an 83 kD form of Stat3 that proved to be the human homologue of a
short form of Stat3, Stat3 beta. Because the transcriptional activity of
Stat3 beta is distinct from Stat3 alpha, these results suggest that the
balance of the two Stat3 isoforms in myeloid cells may influence the
cellular pattern of gene activation and consequently the ability of these
cells to differentiate in response to G-CSF.
Volume 88,
Issue 7,
pp. 2442-2449,
10/01/1996
Copyright © 1996 by The American Society of Hematology
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