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Human acute myeloid leukemia cells bind to bone marrow stroma via a
combination of beta-1 and beta-2 integrin mechanisms
LJ Bendall, K Kortlepel and DJ Gottlieb
Department of Haematology, Westmead Hospital, Westmead New South Wales,
Sydney, Australia.
Acute myeloid leukemia (AML) cells respond to exogenous stimulation from
myeloid growth factors that may be secreted by cells of the bone marrow
(BM) stroma and retained by glycosaminoglycans in the extracellular matrix.
We have analyzed the capacity of malignant cells from patients with AML to
maintain close proximity to sites of growth factor production and retention
by binding to BM stromal elements, including fibroblasts and extracellular
matrix proteins. Leukemic cells from all cases of AML adhered to BM
fibroblast (BMF) monolayers (mean +/- standard error [SE] percentage
binding, 30.9% +/- 2.5%; n = 23) and to fibronectin and laminin (mean +/-
SE percentage binding, 28.0% +/- 4.1% [n = 11] and 21.5% +/- 2.3% [n = 8],
respectively). Binding to bovine and human collagen type 1, vitronectin,
hyaluronic acid, and albumin was minimal. Analysis of binding mechanisms
indicated that very late antigen-4 (VLA-4) and VLA-5 were responsible for
AML cell binding to fibronectin. Binding to laminin could be inhibited by
antibody to the alpha chain of VLA-6. In contrast, AML cell adhesion to BMF
monolayers was not impaired by blocking antibodies to either beta 1 or beta
2 integrins used alone, although the combination of anti-CD11/CD18 and
anti-VLA-4 inhibited binding in more than 50% of cases. When anti- VLA-5
was added in these cases, mean +/- SE inhibition of binding of 45.5% +/-
9.1% (P < .001) was observed. Binding of AML cells to extracellular
matrix proteins fibronectin and laminin is predominantly beta
1-integrin-dependent, but AML cell adhesion to BMF relies on the
simultaneous involvement of beta 1 and beta 2 integrins as well as other
currently unrecognized ligands.
Volume 82,
Issue 10,
pp. 3125-3132,
11/15/1993
Copyright © 1993 by The American Society of Hematology
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