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Prepublished online as a Blood First Edition Paper on April 17, 2002; DOI 10.1182/blood-2001-12-0271.
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Blood, 1 June 2002, Vol. 99, No. 11, pp. 4030-4038
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Normal hemostasis but defective hematopoietic response to growth
factors in mice deficient in phospholipid scramblase 1
Quansheng Zhou,
Ji Zhao,
Therese Wiedmer, and
Peter J. Sims
From the Department of Molecular and Experimental
Medicine and the Department of Vascular Biology, The Scripps Research
Institute, La Jolla, CA.
Phospholipid scramblase 1 (PLSCR1) is an endofacial plasma
membrane protein proposed to participate in transbilayer movement of
phosphatidylserine and other phospholipids. In addition to its putative
role in the reorganization of plasma membrane phospholipids, PLSCR1 is
a substrate of intracellular kinases that imply its possible
participation in diverse signaling pathways underlying proliferation,
differentiation, or apoptosis. Because PLSCR1 is prominently expressed
in a variety of blood cells, we evaluated PLSCR activity in platelets
and erythrocytes, and cytokine-dependent growth of hematopoietic
precursor cells, of PLSCR1 knock-out mice. Adult
PLSCR1 / mice showed no obvious hematologic or
hemostatic abnormality, and blood cells from these animals normally
mobilized phosphatidylserine to the cell surface upon stimulation.
Whereas blood cell counts in adult PLSCR1/ mice were
normal, in both fetus and newborn animals neutrophil counts were
significantly depressed relative to age-matched wild type (WT).
Furthermore, when compared with WT, hematopoietic precursor cells from
PLSCR1/ mice showed defective colony formation and
impaired differentiation to mature granulocytes as stimulated by stem
cell factor and granulocyte colony-stimulating factor (G-CSF). By
contrast, PLSCR1/ cells showed normal colony formation
stimulated by interleukin-3 or granulocyte-macrophage CSF, and
expansion of megakaryocytic and erythroid progenitors by thrombopoietin
or erythropoietin was unaffected. Stem cell factor and G-CSF were also
found to induce marked increases in PLSCR1 levels in WT cells.
Consistent with in vitro assays, PLSCR1/ mice treated
with G-CSF showed less than 50% of the granulocytosis observed in
identically treated WT mice. These data provide direct evidence that
PLSCR1 functionally contributes to cytokine-regulated cell
proliferation and differentiation and suggest it is required for normal myelopoiesis.
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