期刊
BLOOD
卷 112, 期 10, 页码 4048-4050出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2008-07-166587
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资金
- Fonds voor Wetenschappelijk Onderzoek Vlaanderen (FWO) [G.0209.07]
- Belgian Science Policy [IAP-P5/02]
- Bristol-Myers-Squibb grant
- Belgian Instituut voor de Aanmoediging van Innovatie door Wetenschap en Technologie (IWT)
The role of proteinases in the mobilization of hematopoietic progenitor cells (HPCs) after granulocyte colony-stimulating factor (G-CSF) remains unclear. Here we report that genetic loss of the plasminogen activator inhibitor Pai-1 or of the plasmin inhibitor alpha 2-antiplasmin increases HPC mobilization in response to G-CSF. Moreover, thrombolytic agents, such as tenecteplase and microplasmin, enhance HPC mobilization in mice and humans. Taken together, these findings identify a novel role for plasmin in augmenting HPC mobilization in response to G-CSF. (Blood. 2008; 112: 4048-4050)
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