2007
DOI: 10.1182/blood-2007-01-069104
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Hypoxic stress underlies defects in erythroblast islands in the Rb-null mouse

Abstract: 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 eryt… Show more

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Cited by 21 publications
(31 citation statements)
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“…They also used microarray data and quantitative real-time PCR to examine how loss of Rb affected expression of macrophage-specific genes that have been implicated in the erythroblastic island defect in Rb-null fetal livers, including c-Fms, myeloperoxidase, cathepsin S, complement components, and lysozyme. In contrast to the effect of Rb loss on hypoxia-inducible gene expression, they failed to detect any significant change in the expression levels of most macrophage-specific genes in Rb-null fetal liver relative to wild type at E12.5 (Spike et al, 2007). Expression of c-Fms (a PU1 target gene) was previously shown to be deregulated in Rb-null MEFs, and together with data implicating deregulated PU1 in erythroblastic island defects in Rb-null fetal liver was taken as evidence that macrophages were not functioning normally in Rb-null fetal liver (Iavarone et al, 2004).…”
Section: Macrophages Promote Enucleationmentioning
confidence: 81%
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“…They also used microarray data and quantitative real-time PCR to examine how loss of Rb affected expression of macrophage-specific genes that have been implicated in the erythroblastic island defect in Rb-null fetal livers, including c-Fms, myeloperoxidase, cathepsin S, complement components, and lysozyme. In contrast to the effect of Rb loss on hypoxia-inducible gene expression, they failed to detect any significant change in the expression levels of most macrophage-specific genes in Rb-null fetal liver relative to wild type at E12.5 (Spike et al, 2007). Expression of c-Fms (a PU1 target gene) was previously shown to be deregulated in Rb-null MEFs, and together with data implicating deregulated PU1 in erythroblastic island defects in Rb-null fetal liver was taken as evidence that macrophages were not functioning normally in Rb-null fetal liver (Iavarone et al, 2004).…”
Section: Macrophages Promote Enucleationmentioning
confidence: 81%
“…This is specifically true under conditions of oxidative or proliferative stress. Spike et al (2007) argue that it is unlikely that Rb plays a specific role in maintaining erythroblastic island integrity as was originally concluded from the examination Rb-null fetal livers. They suggest that the disruption in erythroblastic island formation is a direct result of hypoxia.…”
Section: Macrophages Promote Enucleationmentioning
confidence: 99%
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“…Although a role for macrophages in definitive erythroid cell maturation is well accepted, 56 several lines of evidence suggest that macrophages are not essential for their enucleation in vivo. 58 Enhancement of EryP enucleation during coculture on fetal liver macrophages was detected in one study 55 but not in another. 42 Nevertheless, interactions with macrophages may facilitate other aspects of erythroid maturation.…”
Section: Niches For Primitive Erythroid Maturation and Enucleationmentioning
confidence: 99%
“…The central macrophages of the EBI are thought to function as nurse cells during erythropoiesis and to provide an essential scavenger function, engulfing nuclei expelled from the maturing erythroblasts (reviewed in refs. [8][9][10].…”
mentioning
confidence: 99%