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Induced expression of c-fms in normal hematopoietic cells shows evidence
for both conservation and lineage restriction of signal transduction in
response to macrophage colony-stimulating factor
GA McArthur, LR Rohrschneider and GR Johnson
Walter and Eliza Hall Institute of Medical Research, Royal Melbourne
Hospital, Victoria, Australia.
Retrovirus-mediated gene transfer was used to obtain expression of the
macrophage colony-stimulating factor (MCSF) receptor, c-fms, on
hematopoietic lineages that normally do not express this receptor. Cultures
of murine fetal liver cells infected with the c-fms retrovirus developed
erythroid colonies in cultures stimulated with M-CSF. However, these
colonies were fewer and less hemoglobinized than colonies in parallel
cultures stimulated by erythropoietin. Culture of isolated clones
demonstrated a direct action of M-CSF on erythroid clones. Culture of c-fms
retrovirus-infected adult murine bone marrow cells showed megakaryocyte and
novel macrophage-megakaryocyte clones when stimulated by M-CSF. Culture of
isolated clones again confirmed a direct action of M-CSF on megakaryocyte
clones. In contrast, M-CSF stimulation of c-fms-infected granulocytes and
granulocyte progenitor cells did not elicit proliferation, enhanced
survival, or functional stimulation of granulocytes. These findings provide
evidence for both conservation and lineage restriction of signal
transduction in normal hematopoietic cells.
Volume 83,
Issue 4,
pp. 972-981,
02/15/1994
Copyright © 1994 by The American Society of Hematology

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