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Blood, 1 November 2005, Vol. 106, No. 9, pp. 3020-3027. Prepublished online as a Blood First Edition Paper on July 21, 2005; DOI 10.1182/blood-2004-01-0272. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-01-0272v1 106/9/3020    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Semerad, C. L. Articles by Link, D. C. Search for Related Content PubMed PubMed Citation Articles by Semerad, C. L. Articles by Link, D. C. Related Collections Hematopoiesis and Stem Cells Cell Adhesion and Motility Gene Expression Chemokines, Cytokines, and Interleukins Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS G-CSF potently inhibits osteoblast activity and CXCL12 mRNA expression in the bone marrow Craig L. Semerad, Matthew J. Christopher, Fulu Liu, Brenton Short, Paul J. Simmons, Ingrid Winkler, Jean-Pierre Levesque, Jean Chappel, F. Patrick Ross, and Daniel C. Link From the Division of Oncology, Department of Internal Medicine and Department of Pathology and Immunology, Washington University School of Medicine, St Louis, MO; Stem Cell Biology Laboratory, Peter MacCallum Cancer Institute, East Melbourne, Victoria, Australia; and Cancer Biotherapy Laboratory, Haematopoietic Stem Cell Team, Mater Medical Research Institute, South Brisbane, Queensland, Australia. Accumulating evidence indicates that interaction of stromal cell-derived factor 1 (SDF-1/CXCL12 [CXC motif, ligand 12]) with its cognate receptor, CXCR4 (CXC motif, receptor 4), generates signals that regulate hematopoietic progenitor cell (HPC) trafficking in the bone marrow. During granulocyte colony-stimulating factor (G-CSF)–induced HPC mobilization, CXCL12 protein expression in the bone marrow decreases. Herein, we show that in a series of transgenic mice carrying targeted mutations of their G-CSF receptor and displaying markedly different G-CSF–induced HPC mobilization responses, the decrease in bone marrow CXCL12 protein expression closely correlates with the degree of HPC mobilization. G-CSF treatment induced a decrease in bone marrow CXCL12 mRNA that closely mirrored the fall in CXCL12 protein. Cell sorting experiments showed that osteoblasts and to a lesser degree endothelial cells are the major sources of CXCL12 production in the bone marrow. Interestingly, osteoblast activity, as measured by histomorphometry and osteocalcin expression, is strongly down-regulated during G-CSF treatment. However, the G-CSF receptor is not expressed on osteoblasts; accordingly, G-CSF had no direct effect on osteoblast function. Collectively, these data suggest a model in which G-CSF, through an indirect mechanism, potently inhibits osteoblast activity resulting in decreased CXCL12 expression in the bone marrow. The consequent attenuation of CXCR4 signaling ultimately leads to HPC mobilization. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. J. Christopher, F. Liu, M. J. Hilton, F. Long, and D. C. Link Suppression of CXCL12 production by bone marrow osteoblasts is a common and critical pathway for cytokine-induced mobilization Blood, August 13, 2009; 114(7): 1331 - 1339. [Abstract] [Full Text] [PDF] B. Nervi, P. Ramirez, M. P. Rettig, G. L. Uy, M. S. 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