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Volume 16, Number 22,
Issue of November 15, 1996
pp. 7240-7252
Copyright ©1996 Society for Neuroscience
A Role in Migration for the  v 1 Integrin Expressed on
Oligodendrocyte Precursors
Received July 29, 1996; revised Aug. 29, 1996; accepted Sept. 4, 1996.
Richard Milner1,
Gwynneth Edwards2,
Charles Streuli2, and
Charles ffrench-Constant1, 3
1 Wellcome/Cancer Research Campaign Institute of
Developmental Biology and Cancer, Cambridge CB2 1QR, United Kingdom,
and Department of Medical Genetics, University of Cambridge, Cambridge
CB2 1QR, United Kingdom, 2 Department of Cell and
Structural Biology, School of Biological Sciences, University of
Manchester, Manchester M13 9PT, United Kingdom, and
3 Medical Research Council Cambridge Center for Brain
Repair, University Forvie Site, Cambridge CB2 2QQ, United Kingdom
Myelination of the CNS requires the migration of oligodendrocyte
precursors throughout the CNS from restricted regions within the
ventricular and subventricular zones. In light of the significant
effects of cell-extracellular matrix (ECM) interactions on cell
migration in other developing systems, we have analyzed the role of
integrins in oligodendrocyte precursor migration. We have shown
previously that oligodendrocyte precursors in vitro
express a limited repertoire of integrins, including  6 1,
v1, and v3, and that differentiation is associated with
downregulation of v1 and upregulation of v5. Using a
migration assay based on the movement of cells away from an agarose
drop containing a high-density cell suspension, we find that RGD
peptides (that block v but not 6 integrins) and anti-1
antibodies block migration on an astrocyte-derived ECM, whereas
anti-3 antibodies have little effect. These re- sults
suggest that v1 but not 61 plays a role in oligodendrocyte
precursor migration, and this is confirmed by the use of blocking
monoclonal antibodies that distinguish these two integrins. In keeping
with the results of others, we find that differentiated
oligodendrocytes lose migratory potential and that the timing of this
loss correlates with downregulation of v1. Taken together with
the work of others showing that ECM ligands for v1 are expressed
within the CNS, we propose that this integrin plays a significant role
in the migration of oligodendrocyte precursors in vivo
and that its downregulation during differentiation could be an
important factor regulating the migratory phenotype of these cells.
Key words:
oligodendrocyte;
integrin;
extracellular matrix;
platelet-derived growth factor;
differentiation;
migration;
astroglial
matrix;
vitronectin
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