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G-CSF down-regulation of CXCR4 expression identified as a mechanism for mobilization of myeloid cells
Cited 156 time in
Web of Science
Cited 162 time in Scopus
- Authors
- Issue Date
- 2006-08-01
- Publisher
- American Society of Hematology
- Citation
- Blood. 2006;108:812-820
- Keywords
- Bone Marrow Cells ; Chemokine CXCL12 ; Chemokines, CXC/physiology ; Down-Regulation/*drug effects/genetics ; Granulocyte Colony-Stimulating Factor/administration & ; dosage/*pharmacology ; Hematopoietic Stem Cell Mobilization/*methods ; Mice, Inbred C57BL ; Myeloid Cells/drug effects/metabolism ; Receptors, CXCR4/*drug effects/genetics
- Abstract
- CXCR4 receptor expression is required for the retention of granulocyte precursors and mature neutrophils within the bone marrow, and disruption of the SDF-1/CXCR4 axis in the bone marrow results in the mobilization of myeloid lineage cells to the peripheral circulation. We report that G-CSF down-regulates CXCR4 expression in bone marrow-derived murine and human myeloid lineage cells. When exposed to G-CSF, murine Gr1(+) bone marrow myeloid cells display a time-dependent reduction of cell-surface CXCR4 and respond poorly to SDF-1 in attachment and migration assays. Bone marrow-derived cells of nonmyeloid lineage display no change in surface CXCR4 expression upon exposure to G-CSF. Compared with controls, mice treated with G-CSF for mobilization of hematopoietic progenitor cells display reduced levels of CXCR4 selectively in bone marrow Gr1(+) myeloid cells. Since bone marrow myeloid cells express G-CSF receptors and G-CSF rapidly reduces CXCR4 expression in purified Gr1(+) cells populations, these results provide evidence that G-CSF acts directly on myeloid lineage cells to reduce CXCR4 expression. By down-regulating CXCR4 expression in bone marrow myeloid cells and attenuating their responsiveness to SDF-1, G-CSF promotes their mobilization from the bone marrow to the peripheral blood.
- ISSN
- 0006-4971 (Print)
- Language
- English
- URI
- http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16537807
https://hdl.handle.net/10371/11870
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