Abstract
Haematopoietic stem and progenitor cells move from the bone marrow into the circulation to replenish normal blood-cell levels. Inhibiting a prostaglandin-mediated signalling pathway may promote this process. See Letter p.365 The haematopoietic stem cell (HSC) microenvironment supports progenitor cells producing new circulating blood cells yet prevents the inappropriate exit of immature cells into the bloodstream. This study identifies endogenous prostaglandin E2 (PGE2) as a component in the maintenance of this delicate balance. Louis M. Pelus and colleagues show that inhibition of endogenous PGE2 signalling by nonsteroidal anti-inflammatory drugs (NSAIDs) significantly increases the release of functional haematopoietic stem and progenitors from bone marrow into the peripheral blood, with additive effects when used in conjunction with granulocyte colony-stimulating factor. Tests in primates and human volunteers suggest a strategy that might be used therapeutically to enhance transplantation survival: administration of NSAIDs (aspirin, ibuprofen and meloxicam) enhances stem-cell mobilization, with faster haematologic recovery and enhanced long-term stem-cell repopulation of haematopoietic grafts.
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