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Blood, Vol. 95 No. 10 (May 15), 2000:
pp. 3025-3031
PLENARY PAPER
Expression of the G-CSF receptor on hematopoietic progenitor
cells is not required for their mobilization by G-CSF
Fulu Liu,
Jennifer Poursine-Laurent, and
Daniel C. Link
From the Washington University School of Medicine, Division of Bone
Marrow Transplantation and Stem Cell Biology, Department of Internal
Medicine, St. Louis, MO.
The mechanisms that regulate hematopoietic progenitor cell (HPC)
mobilization from the bone marrow to blood have not yet been defined. HPC mobilization by granulocyte colony-stimulating factor (G-CSF), cyclophosphamide (CY), or interleukin-8 but
not flt-3 ligand is markedly impaired in G-CSF
receptor-deficient (G-CSFR-deficient) mice. G-CSFR is expressed on
mature hematopoietic cells, HPCs, and stromal cells, which
suggests that G-CSFR signals in one or more of these cell types was
required for mobilization by these agents. To define the cell type(s)
responsible for G-CSF-dependent mobilization, a series of chimeric
mice were generated using bone marrow transplantation. Mobilization
studies in these chimeras demonstrated that expression of the G-CSFR on
transplantable hematopoietic cells but not stromal cells is required
for CY- or G-CSF-induced mobilization. Moreover, in irradiated mice
reconstituted with both wild type and G-CSFR-deficient bone marrow
cells, treatment with CY or G-CSF resulted in the equal mobilization of
both types of HPCs. This result held true for a broad spectrum of HPCs
including colony-forming cells, CD34+
lineage and Sca+ lineage
cells, and long-term culture initiating cells. Collectively, these data
provide the first definitive evidence that expression of the G-CSFR on
HPCs is not required for their mobilization by G-CSF and suggest a
model in which G-CSFR-dependent signals act in trans to
mobilize HPCs from the bone marrow.
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