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Expression of human colony-stimulating factor-1 (CSF-1) receptor in murine
pluripotent hematopoietic NFS-60 cells induces long-term proliferation in
response to CSF-1 without loss of erythroid differentiation potential
RP Bourette, G Mouchiroud, R Ouazana, F Morle, J Godet and JP Blanchet
Centre de Genetique Moleculaire et Cellulaire, UMR CNRS no. 106, Universite
Claude Bernard Lyon I, Villeurbanne, France.
NFS-60 and FDCP-Mix cells are interleukin-3--dependent multipotent
hematopoietic cells that can differentiate in vitro into mature myeloid and
erythroid cells. Retrovirus-mediated transfer of the human colony-
stimulating factor-1 (CSF-1) receptor gene (c-fms) enabled NFS-60 cells but
not FDCP-Mix cells to proliferate in response to CSF-1. The phenotype of
NFS-60 cells expressing the human CSF-1 receptor (CSF-1R) grown in CSF-1
did not grossly differ from that of original NFS-60 as assessed by
cytochemical and surface markers. Importantly, these cells retained their
erythroid potentiality. In contrast, a CSF-1-dependent variant of NFS-60,
strongly expressing murine CSF-1R, differentiated into monocyte/macrophages
upon CSF-1 stimulation and almost totally lost its erythroid potentiality.
We also observed that NFS-60 but not FDCP-Mix cells could grow in response
to stem cell factor, (SCF), although both cell lines express relatively
high amounts of SCF receptors. This suggests that SCF-R and CSF-1R
signalling pathways share at least one component that may be missing or
insufficiently expressed in FDCP-Mix cells. Taken together, these results
suggest that human CSF-1R can use the SCF-R signalling pathway in murine
multipotent cells and thereby favor self-renewal versus differentiation.
Volume 81,
Issue 10,
pp. 2511-2520,
05/15/1993
Copyright © 1993 by The American Society of Hematology
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