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Vol. 13, No. 19, pp. 2478-2483, October 1, 1999
1 Department of Pathology, 2 Committee on Cancer
Biology, 3 Departments of Medicine and Molecular Genetics and
Cell Biology, and the Howard Hughes Medical Institute (HHMI),
University of Chicago, Chicago, Illinois 60637 USA
Although most cells undergo growth arrest during hypoxia,
endothelial cells and placental cytotrophoblasts proliferate in response to low O2. We demonstrate that proliferation of
embryonic multilineage hematopoietic progenitors is also regulated by a hypoxia-mediated signaling pathway. This pathway requires HIF-1 (HIF-1
/ARNT heterodimers) because Arnt
/
embryoid bodies fail to exhibit hypoxia-mediated progenitor proliferation. Furthermore, Arnt/ embryos exhibit decreased
numbers of yolk sac hematopoietic progenitors. This defect is cell
extrinsic, is accompanied by a decrease in ARNT-dependent VEGF
expression, and is rescued by exogenous VEGF. Therefore, "physiologic
hypoxia" encountered by embryos is essential for the proliferation or
survival of hematopoietic precursors during development.
[Key Words: ARNT; HIF; hypoxia; hematopoiesis; VEGF; embryoid body; ES cells]
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