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Disruption of the CXCR4/CXCL12 chemotactic interaction during hematopoietic stem cell mobilization induced by GCSF or cyclophosphamide
Breaking the CXCR4/CXCL12 signaling during blood stem cell release caused by GCSF or cyclophosphamide
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Abstract
Mobilization of hematopoietic progenitor cells (HPCs) by GCSF is associated with the cleavage of the CXCR4 receptor on these cells.
- Cleavage of CXCR4 on HPCs leads to a loss of their ability to respond to the chemokine SDF-1.
- Concentrations of SDF-1 in the bone marrow decrease during the mobilization of HPCs.
- This decrease in SDF-1 coincides with the accumulation of serine proteases that can cleave and inactivate SDF-1.
- Both SDF-1 and CXCR4 are crucial for the retention of HPCs in the bone marrow.
- The degradation of SDF-1 and CXCR4 may be a key factor in the process of HPC mobilization into peripheral blood.
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