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Blood, 15 September 2007, Vol. 110, No. 6, pp. 2173-2181.
Prepublished online as a Blood First Edition Paper on June 8, 2007; DOI 10.1182/blood-2007-01-069104.
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RED CELLS
Hypoxic stress underlies defects in erythroblast islands in the Rb-null mouse
Benjamin T. Spike1,2,
Benjamin C. Dibling1, and
Kay F. Macleod1,2
1 Ben May Department for Cancer Research, Center for Integrative Sciences, Chicago, IL;
2 Committee on Cancer Biology, University of Chicago, IL
Definitive erythropoiesis occurs in islands composed of a central macrophage in contact with differentiating erythroblasts. Erythroid maturation including enucleation can also occur in the absence of macrophages both in vivo and in vitro. We reported previously that loss of Rb induces cell-autonomous defects in red cell maturation under stress conditions, while other reports have suggested that the failure of Rb-null erythroblasts to enucleate is due to defects in associated macrophages. Here we show that erythropoietic islands are disrupted by hypoxic stress, such as occurs in the Rb-null fetal liver, that Rb–/– macrophages are competent for erythropoietic island formation in the absence of exogenous stress and that enucleation defects persist in Rb-null erythroblasts irrespective of macrophage function.
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