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Plasmin therapy enhances mobilization of HPCs after G-CSF.

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 alpha2-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.

SUBMITTER: Tjwa M

PROVIDER: S-EPMC2581978 | biostudies-literature | 2008 Nov

REPOSITORIES: biostudies-literature

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Plasmin therapy enhances mobilization of HPCs after G-CSF.

Tjwa Marc M Janssens Stefan S Carmeliet Peter P

Blood 20080822 10

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 alpha2-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 ...[more]

PMID: 18723692

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