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Prepublished online as a Blood First Edition Paper on May 22, 2003; DOI 10.1182/blood-2003-04-1212.
Submitted April 22, 2003
Accepted May 9, 2003
PSGL-1 participates in E-selectin-mediated progenitor homing to bone marrow: evidence for cooperation between E-selectin ligands and  4 integrin
Yoshio Katayama, Andres Hidalgo, Barbara C Furie, Dietmar Vestweber, Bruce Furie, and Paul S Frenette*
Department of Medicine, Mount Sinai School of Medicine, New York, NY, USA
Center for Hemostasis and Thrombosis, Harvard Medical School, Boston, MA, USA
Institute of Cell Biology, University of Munster, Munster, Germany
* Corresponding author; email: paul.frenette{at}mssm.edu.
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 (~35% reduction 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 (~55% reduction). 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 pre-treated 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.
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