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Blood, 1 January 2006, Vol. 107, No. 1, pp. 79-86. Prepublished online as a Blood First Edition Paper on September 1, 2005; DOI 10.1182/blood-2005-05-2023. This Article Full Text Full Text (PDF) All Versions of this Article: 2005-05-2023v1 107/1/79    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 Bonig, H. Articles by Papayannopoulou, T. Search for Related Content PubMed PubMed Citation Articles by Bonig, H. Articles by Papayannopoulou, T. Related Collections Hematopoiesis and Stem Cells Cell Adhesion and Motility Signal Transduction Stem Cells in Hematology Chemokines, Cytokines, and Interleukins Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS Hierarchy of molecular-pathway usage in bone marrow homing and its shift by cytokines Halvard Bonig, Gregory V. Priestley, and Thalia Papayannopoulou From the Department of Medicine/Hematology, University of Washington, Seattle, WA. Efficient bone marrow (BM) homing is a prerequisite for successful engraftment of transplanted hematopoietic cells (HPCs). Contradictory conclusions about the contribution of SDF-1/CXCR4 have clouded our understanding of its role within the molecular pathway cooperation needed for BM homing, particularly with the well-defined hierarchic network of adhesion molecules. In the present study we sought to unravel cooperative and compensatory molecular pathways guiding BM homing. Fresh BM-HPCs, rendered either SDF-1 unresponsive or Gi-signaling refractory, homed quite efficiently, because of compensation by 4-integrin interacting with VCAM-1. The contribution of SDF-1/CXCR4- or Gi-protein-mediated signals to BM homing became apparent after their blockade was combined with deletion of 4-integrin, leading to dramatic reduction in BM homing. Similar conclusions were revealed when VCAM-1-deficient hosts were used. Cytokine incubation changed the functional properties of BM-HPCs and hierarchy of molecular pathway usage in homing, by shifting the dominance among the homing mediators: loss of CXCR4 or Gi-signaling now significantly reduced BM homing, with only partial compensation through 4/VCAM-1 and endothelial selectins. These studies depict a flexible hierarchy of cooperating homing pathways, in which dominant players are repositioned with changing cytokine milieu, and possibly source of HPCs. 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