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Blood, 1 June 2002, Vol. 99, No. 11, pp. 4182-4191
TRANSPLANTATION
Total body irradiation causes profound changes in endothelial
traffic molecules for hematopoietic progenitor cell recruitment to
bone marrow
Irina B. Mazo,
Elizabeth J. Quackenbush,
John B. Lowe, and
Ulrich H. von
Andrian
From the Center for Blood Research, the Department of
Pathology, and the Division of Clinical Genetics, Children's Hospital,
Harvard Medical School, Boston, MA; and the Howard Hughes Medical
Institute, University of Michigan, Ann Arbor.
Nonirradiated bone marrow (BM) venules and sinusoids in murine
skull support hematopoietic progenitor cell (HPC) rolling through constitutively expressed endothelial (P- and E-) selectins and VCAM-1.
Using intravital microscopy, we tested whether host conditioning with
total body irradiation (TBI) changes the molecular mechanisms by which
murine HPCs from fetal livers (FL) interact with BM endothelial cells.
Although a high dose of TBI did not affect the overall frequency of HPC
rolling in BM microvessels, the underlying molecular mechanisms
differed from those in nonirradiated BM. TBI induced VCAM-1
up-regulation in BM microvessels, whereas P-selectin expression was
reduced and the low baseline level of E-selectin remained unchanged.
Only the administration of anti-VCAM-1, but not anti-P- or
-E-selectin monoclonal antibodies, decreased FL HPC rolling. Rolling
was frequently followed by firm arrest (sticking), even in
nonirradiated BM microvessels in which sticking was entirely pertussis
toxin-insensitive that is, G i-coupled signaling events (eg, through chemokines) were apparently not required. TBI increased the frequency of sticking FL HPC. This irradiation-induced additional sticking was reversed when FL HPCs were pretreated with pertussis toxin, suggesting that TBI induced elevated expression of a
Gi-protein-coupled chemotactic signal in the BM. This
chemoattractant was probably distinct from SDF-1 because, unlike
adult HPCs, FL HPCs (day 11 of gestation) responded poorly to SDF-1
in vitro. These results demonstrate that TBI induces profound changes
in the expression of endothelial traffic molecules in the BM, and they
indicate that FL HPCs can home to the BM in the absence of SDF-1 and
other Gi-protein-coupled signals.
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