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J Biol Chem, Vol. 274, Issue 8, 4816-4823, February 19, 1999
From the Division of Preventive Medicine and Department of
Medicine, Columbia University College of Physicians and Surgeons,
New York, New York 10032
Reduced heparin and heparan sulfate (HS)
proteoglycans (PG) have been observed in both inflammation and
atherosclerosis. Methods to increase endogenous heparin and heparan
sulfate are not known. We found that incubation of endothelial cells
with 500-1,000 µg/ml high density lipoprotein (HDL) increased
35SO4 incorporation into PG by
1.5-2.5-fold. A major portion of this increase was in HS and was the
result of increased synthesis. Total PG core proteins were not altered
by HDL; however, the ratio of 35SO4 to
[3H]glucosamine was increased by HDL, suggesting
increased sulfation of glycosaminoglycans. In addition, HDL increased
the amount of highly sulfated heparin-like HS in the subendothelial
matrix. HS from HDL-treated cells bound 40 ± 5% more
125I-antithrombin III (requires 3-O sulfated
HS) and 49 ± 3% fewer monocytes. Moreover, the HS isolated from
HDL-treated cells inhibited smooth muscle cell proliferation (by
83 ± 5%) better than control HS (56 ± 6%) and heparin
(42 ± 6%). HDL isolated from apolipoprotein E (apoE)-null mice
did not stimulate HS production unless apoE was added. ApoE also
stimulated HS production in the absence of HDL. ApoE did not increase
35SO4 incorporation in macrophages and
fibroblasts, suggesting that this is an endothelial cell-specific
process. Receptor-associated protein inhibited apoE-mediated
stimulation of HS only at higher (20 µg/ml) doses, suggesting the
involvement of a receptor-associated protein-sensitive pathway in
mediating apoE actions. In summary, our data identify a novel mechanism
by which apoE and apoE-containing HDL can be anti-atherogenic.
Identification of specific apoE peptides that stimulate endothelial
heparin/HS production may have important therapeutic applications.
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