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*
Department of Experimental Immunohematology, CLB and Laboratory for Experimental and Clinical Immunology, and
Department of Hematology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
The success of stem cell transplantation depends on the ability of
i.v. infused stem cells to engraft the bone marrow, a process referred
to as homing. Efficient homing requires migration of CD34+
cells across the bone marrow endothelium, most likely through the
intercellular junctions. In this study, we show that loss of vascular
endothelial (VE)-cadherin-mediated endothelial cell-cell adhesion
increases the permeability of monolayers of human bone marrow
endothelial cells (HBMECs) and stimulates the transendothelial
migration of CD34+ cells in response to stromal
cell-derived factor-1
. Stromal cell-derived factor-1-induced
migration was dependent on VCAM-1 and ICAM-1, even in the absence of
VE-cadherin function. Cross-linking of ICAM-1 to mimic the
leukocyte-endothelium interaction induced actin stress fiber formation
but did not induce loss of endothelial integrity, whereas cross-linking
of VCAM-1 increased the HBMEC permeability and induced gaps in the
monolayer. In addition, VCAM-1-mediated gap formation in HBMEC was
accompanied by and dependent on the production of reactive oxygen
species. These data suggest that modulation of VE-cadherin function
directly affects the efficiency of transendothelial migration of
CD34+ cells and that activation of ICAM-1 and, in
particular, VCAM-1 plays an important role in this process through
reorganization of the endothelial actin cytoskeleton and by modulating
the integrity of the bone marrow endothelium through the production of
reactive oxygen species.
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