Plasmin therapy enhances mobilization of HPCs after G-CSF
M Tjwa, S Janssens, P Carmeliet - Blood, The Journal of the …, 2008 - ashpublications.org
M Tjwa, S Janssens, P Carmeliet
Blood, The Journal of the American Society of Hematology, 2008•ashpublications.orgThe 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 α2-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 …
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 α2-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 …
Abstract
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 α2-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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