Hematopoietic Stem Cells |
4 integrin- and CXCR4-mediated engraftment in NOD/SCID β2-microglobulin-null miceGIGA-Research, Hematology Unit, University of Liège, Belgium
Correspondence: André Gothot, M.D., University of Liège, Laboratory Hematology CHU Sart Tilman B35 13, avenue de lHôpital B-4000 Liège, Belgium E-mail:agothot{at}ulg.ac.be
Background: Several studies indicate that ex vivo cytokine-supported expansion induces defective hematopoietic stem cell engraftment. We investigated the role of
4 integrin,
5 integrin and CXCR4 in engraftment of unmanipulated and cytokine-treated human cord blood CD34+ cells.
Design and Methods: Uncultured or expanded CD34+ cells were infused in NOD/SCID-β2microglobulin-null mice. The function of
4, and
5 integrins and CXCR4 was assessed by incubating cells with specific neutralizing antibodies, prior to transplant. The activation state of
4 integrin was further tested by adhesion and migration assays.
Results: Neutralization of either
4 integrin or CXCR4 abolished engraftment of uncultured CD34+ cells at 6 week spost-transplant, while
5 integrin neutralization had no significant effect. However, after short-term ex vivo culture, blocking
4 integrin or CXCR4 did not affect repopulating activity whereas neutralization of
5 integrin inhibited engraftment. Using soluble vascular cell adhesion molecule-1 binding assays, we observed that
4 integrin affinity in fresh CD34+ cells was low and susceptible to stimulation while in cultured CD34+ cells, it was high and insensitive to further activation. In addition, stromal cell-derived factor-1 stimulated migration across vascular cell adhesion molecule-1 in fresh CD34+ cells but not in cultured CD34+ cells.
Conclusions: Our data show that ex vivo culture of hematopoietic progenitor cells is associated with downregulation of both
4 integrin- and CXCR4-mediated engraftment. Further investigations suggest that this is caused by supraphysiological increase of
4 integrin affinity, which impairs directional migration across vascular cell adhesion molecule-1 in response to stromal cell-derived factor-1. Such changes may underlie the engraftment defect of cytokine-stimulated CD34+ cells.
Key words: stem cells, hematopoiesis, cell trafficking.