Submitted July 2, 2008
Accepted August 13, 2008
Plasmin therapy enhances mobilization of HPCs after G-CSF
Marc Tjwa, Stefan Janssens, and Peter Carmeliet*
Vesalius Research Center, KU Leuven, Leuven, Belgium
Vesalius Research Center, VIB - KU Leuven, Leuven
* Corresponding author; email: peter.carmeliet{at}med.kuleuven.be.
The role of proteinases in the mobilization of hematopoietic progenitor cells (HPCs) after G-CSF remains unclear. Here, we report that genetic loss of the plasmininogen activator inhibitor PAI-1 or of the plasmin inhibitor 
2-antiplasmin increases HPC mobilization in response to G-CSF. Moreover, thrombolytic agents such as tenecteplase and micro-plasmin enhance HPC mobilization in mice and in humans. Taken together, these findings identify a novel role for plasmin in augmenting HPC mobilization in response to G-CSF.
