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J Biol Chem, Vol. 273, Issue 32, 20156-20161, August 7, 1998
From the Department of Pathology and Laboratory Medicine,
University of Cincinnati College of Medicine,
Cincinnati, Ohio 45267-0529
The anti-atherogenic effects of apolipoprotein
(apo) E have been attributed to its ability to reduce plasma
cholesterol level and to limit foam cell formation. The purpose of this
study was to ascertain if apoE also may have cytostatic functions that
could attenuate vascular occlusive diseases. Purified apoE inhibited smooth muscle cell migration directed to platelet-derived growth factor
(PDGF) or oxidized LDL (oxLDL) (p < 0.0001). The
purified apoE also suppressed PDGF- and oxLDL-induced smooth muscle
cell proliferation (p < 0.001). These apoE inhibitory
effects were not because of suppression of PDGF binding to its
receptors on the smooth muscle cells, but was correlated with a
significant reduction in agonist-stimulated mitogen-activated protein
kinase activity (p < 0.01). ApoE also inhibited
PDGF-induced cyclin D1 mRNA expression, suggesting that the apoE
effect was mediated by growth arrest at the G0 to
G1 phase. Taken together, these results suggest that apoE
has cytostatic functions in the vessel wall and may protect against
vascular diseases through inhibition of cell signaling events
associated with growth factor-induced smooth muscle cell migration and
proliferation.
Apolipoprotein E Inhibits Platelet-derived Growth
Factor-induced Vascular Smooth Muscle Cell Migration and
Proliferation by Suppressing Signal Transduction and Preventing Cell
Entry to G1 Phase
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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