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Prepublished online as a Blood First Edition Paper on May 22, 2003; DOI 10.1182/blood-2003-04-1212. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-04-1212v1 102/6/2060    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 Katayama, Y. Articles by Frenette, P. S. Search for Related Content PubMed PubMed Citation Articles by Katayama, Y. Articles by Frenette, P. S. Related Collections Cell Adhesion and Motility Hematopoiesis and Stem Cells Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 September 2003, Vol. 102, No. 6, pp. 2060-2067 HEMATOPOIESIS PSGL-1 participates in E-selectin–mediated progenitor homing to bone marrow: evidence for cooperation between E-selectin ligands and 4 integrin Yoshio Katayama, Andrés Hidalgo, Barbara C. Furie, Dietmar Vestweber, Bruce Furie, and Paul S. Frenette From the Department of Medicine, Mount Sinai School of Medicine, New York, NY; the Institute of Cell Biology, University of Münster, Germany; and the Center for Hemostasis and Thrombosis Research, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA. The nature and exact function of selectin ligands involved in hematopoietic progenitor cell (HPC) homing to the bone marrow (BM) are unclear. Using murine progenitor homing assays in lethally irradiated recipients, we found that the P-selectin glycoprotein ligand-1 (PSGL-1) plays a partial role in HPC homing to the BM (a reduction of about 35% when the P-selectin binding region is blocked). Blockade of both PSGL-1 and 4 integrin did not further enhance the effect of anti-4 integrin (a reduction of about 55%). We suspected that E-selectin ligands might contribute to the remaining homing activity. To test this hypothesis, HPC homing assays were carried out in E-selectin–deficient recipients and revealed a profound alteration in HPC homing when E-selectin and 4 integrin were inactivated (> 90% reduction). Competitive assays to test homing of long-term repopulating stem cells revealed a drastic reduction (> 99%) of the homed stem cell activity when both 4 integrin and E-selectin functions were absent. Further homing studies with PSGL-1–deficient HPCs pretreated with anti-4 integrin antibody revealed that PSGL-1 contributes to approximately 60% of E-selectin ligand–mediated homing activity. Our results thus underscore a major difference between mature myeloid cells and immature stem/progenitor cells in that E-selectin ligands cooperate with 4 integrin rather than P-selectin ligands. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D. D. Wagner and P. S. Frenette The vessel wall and its interactions Blood, June 1, 2008; 111(11): 5271 - 5281. [Abstract] [Full Text] [PDF] E. Galkina and K. Ley Vascular Adhesion Molecules in Atherosclerosis Arterioscler. Thromb. Vasc. Biol., November 1, 2007; 27(11): 2292 - 2301. [Abstract] [Full Text] [PDF] H. Qian, E. Georges-Labouesse, A. Nystrom, A. Domogatskaya, K. Tryggvason, S. E. W. Jacobsen, and M. 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