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Journal of Lipid Research, Vol 24, 1160-1167, Copyright © 1983 by Lipid Research, Inc.
AB Roberts, AM Lees, RS Lees, HW Strauss, JT Fallon, J Taveras and S Kopiwoda
To determine whether damaged arterial wall selectively accumulates
lipoproteins, normocholesterolemic rabbits were injected with human
radiolabeled low density lipoproteins, high density lipoproteins, and/or
albumin 24 hr to 12 weeks after balloon-catheter de- endothelialization of
the abdominal aorta. When 125I-labeled low density lipoproteins and
99mTc-labeled albumin were injected simultaneously, the amount of 125I-low
density lipoprotein present 24 hr later in abdominal aortas increased
steadily, for several weeks, above the amount present at 24 hr in control
animals. The increase correlated closely with the degree of
re-endothelialization and correlated closely with the degree of
re-endothelialization and reached an average maximum for the whole
abdominal aorta of three times control when re-endothelialization was
between 75 and 85% complete. By contrast, the amounts of 99mTc-albumin or
125I-labeled high density lipoprotein in balloon-damaged abdominal aortas,
and the amounts of 125I-low density lipoprotein, 125I-high density
lipoprotein, or 99mTc- albumin in undamaged thoracic aortas of injured
animals showed no such increase. As early as 2 weeks after
de-endothelialization, en face radioautographs made following injection of
125I-labeled low density lipoproteins revealed localized areas of greatest
radioactivity around the leading edges of regenerating endothelial islands,
broad areas of intermediate radioactivity corresponding to the
de-endothelialized areas, and very like radioactivity in the
re-endothelialized areas. This pattern occurred rarely with 125I-labeled
high density lipoproteins and not at all with 125I-labeled albumin. The
results suggest that low density lipoproteins are selectively accumulated
by the healing rabbit aorta and that the accumulation is greatest in
regions where the endothelium is actively regenerating.
ARTICLES
Selective accumulation of low density lipoproteins in damaged arterial wall
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