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Apoptosis

Cutting red-cell production

Nature volume 401, pages 433–435 (1999)Cite this article

For the proper delivery of oxygen to our tissues we need to have enough circulating red blood cells (erythrocytes). As Olympic officials have learned, artificially boosting the number of erythrocytes enhances athletic performance. But a potential downside of having excessive red blood cells is sluggish circulation and stroke. So, for good health, we need finely tuned regulation of red-cell production, and on page 489 of this issue DeMaria and colleagues1 propose a new mechanism for how this might be accomplished.

In mammals, red blood cells form in the bone marrow within anatomical units called erythroblastic islands. These units comprise macrophages (white blood cells that engulf foreign particles and microorganisms) surrounded by erythroblasts at different stages of maturation. The proliferation and survival of these erythroblasts depend on the presence of erythropoietin. Erythroblasts have erythropoietin receptors on their surface and, if deprived of erythropoietin, they succumb to apoptosis. In part, this reflects a requirement for signals from the erythropoietin receptor in inducing or stabilizing the expression of an anti-apoptotic protein called bcl-xL (ref. 2). Indeed, as shown by a study of embryonic stem cells3, bcl-xL is also necessary for normal maturation of erythroid cells. So, as with many other types of cell, apoptosis must be held in check for normal development to ensue.

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Figure 1: Convergence of opposing pathways on the transcription factor GATA-1 to regulate the survival and maturation of red blood cells.

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Authors and Affiliations

  1. Ontogeny Inc., 45 Moulton Street, Cambridge, 02138, Massachusetts, USA

    Stuart H. Orkin & Mitchell J. Weiss

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  1. Stuart H. Orkin
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  2. Mitchell J. Weiss
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Correspondence to Stuart H. Orkin.

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Orkin, S., Weiss, M. Cutting red-cell production. Nature 401, 433–435 (1999). https://doi.org/10.1038/46699

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