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Blood, 1 February 2002, Vol. 99, No. 3, pp. 792-799
CHEMOKINES
Stromal-derived factor 1 inhibits the cycling of very primitive
human hematopoietic cells in vitro and in NOD/SCID mice
Johanne Cashman,
Ian Clark-Lewis,
Allen Eaves, and
Connie Eaves
From the Terry Fox Laboratory, British Columbia Cancer
Agency; and the Departments of Medical Genetics, Biochemistry,
Medicine, and Pathology and Laboratory Medicine, and the Biomedical
Research Centre, University of British Columbia, Vancouver, BC, Canada.
Stromal-derived factor 1 (SDF-1) is a -CXC- chemokine that
plays a critical role in embryonic and adult hematopoiesis, and its
specific receptor, CXCR4, has been implicated in stem cell homing. In
this study, it is shown that the addition of SDF-1 to long-term
cultures (LTCs) of normal human marrow can selectively, reversibly, and
specifically block the S-phase entry of primitive quiescent erythroid
and granulopoietic colony-forming cells (CFCs) present in the adherent
layer. Conversely, addition of anti-SDF-1 antibody or SDF-1(G2), a
specific CXCR4 antagonist, to preactivated human LTCs prevented both
types of primitive CFCs from re-entering a quiescent state,
demonstrating that endogenous SDF-1 contributes to the control of
primitive CFC proliferation in the LTC system. Interestingly, SDF-1
failed to arrest the proliferation of primitive chronic myeloid
leukemia CFCs in the adherent layer of LTCs containing normal marrow
stromal cells. In vivo, injection of SDF-1 arrested the cycling of
normal human LTC-initiating cells as well as primitive CFCs in the
marrow of nonobese diabetic/severe combined
immunodeficient mice engrafted with human cord blood cells.
Conversely, injection of the antagonist, SDF-1(G2), reactivated the
cycling of quiescent primitive human CFCs present in the marrow of mice
engrafted with human marrow cells. These studies are the first to
demonstrate a potential physiological role of SDF-1 in regulating the
cell-cycle status of primitive hematopoietic cells and suggest that the
deregulated cycling activity of primitive chronic myeloid leukemia
(CML) cells is due to the BCR-ABL-mediated disruption of a pathway
shared by multiple chemokine receptors.
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