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Abstract
In this issue of the JCI, Capitano et al. demonstrate that the secreted form of the DNA-binding chromatin factor DEK regulates hematopoiesis. It is known that DEK can be secreted by macrophages and other cells, but no function has been attached to secreted DEK. Capitano et al. showed that extracellular DEK activates signaling through the CXCL2 receptor, which in turn enhances the proliferation of hematopoietic stem cells and decreases hematopoietic progenitor cell numbers both in vivo and in vitro. These results offer the opportunity to expand transplantable stem cells to improve outcomes in patients undergoing bone marrow transplant.
Authors
David M. Bodine
Figure 1
The role of extracellular DEK in hematopoiesis.
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Extracellular DEK engages the CXCR2 receptor and heparan sulfate proteoglycans (HSPG), triggering a signaling cascade that phosphorylates AKT, ERK, and p38 MAPK (center). DEK increases hematopoietic stem cell (HSC) and decreases hematopoietic progenitor cell (HPC) proliferation in vivo and in vitro, with conflicting effects on HSC engraftment (left). Potential clinical applications are shown on the right.
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ISSN: 0021-9738 (print), 1558-8238 (online)