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Blood, 15 November 2008, Vol. 112, No. 10, pp. 4048-4050.
Prepublished online as a Blood First Edition Paper on September 26, 2008; DOI 10.1182/blood-2008-07-166587.


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HEMATOPOIESIS AND STEM CELLS

Brief Report

Plasmin therapy enhances mobilization of HPCs after G-CSF

Marc Tjwa1,2, Stefan Janssens1,2, and Peter Carmeliet1,2

1 Vesalius Research Center, Leuven, Belgium; and 2 Vesalius Research Center Katholieke Universiteit (K.U.) Leuven, Leuven, Belgium

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.


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