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Journal of Lipid Research, Vol 32, 317-327, Copyright © 1991 by Lipid Research, Inc.
JM Pepin, JA O'Neil and HF Hoff
Lipoprotein[a] or Lp[a] is a cholesterol-rich plasma lipoprotein that is
associated with increased risk for cardiovascular disease. To better
understand this association we determined the amount of apo[a] and apoB as
possible estimates for Lp[a] and low density lipoprotein (LDL) accumulation
in atherosclerotic lesions and in plasma, from patients undergoing vascular
surgery, using specific radioimmunoassays for apolipoprotein[a] and
apolipoprotein B. Apo[a] and apoB were operationally divided into a loosely
bound fraction obtained by extracting minced samples of plaque with
phosphate-buffered saline (PBS), and a tightly bound fraction obtained by
extracting the residual tissue with 6 M guanidine-HCl (GuHCl). We found
that 83% of all apo[a] but only 32% of all apoB in lesions was in the
tightly bound fraction. When normalized for corresponding plasma levels,
apo[a] accumulation in plaques was more than twice that of apoB. All
fractions of tissue apo[a], loosely bound, tightly bound, and total,
correlated significantly with plasma apo[a]. However, no significant
correlations were found between any of the tissue fractions and plasma
apoB. If all apo[a] and apoB had been associated with intact Lp[a] or LDL
particles, the calculated mass of tightly bound Lp[a] would actually have
exceeded that of tightly bound LDL in five cases with plasma Lp[a] levels
above 5 mg apo[a] protein/dl. When PBS and GuHCl extracts of lesions were
subjected to one-dimensional electrophoresis, the major band stained for
lipid and immunoblotted positively for apo[a] and apoB, suggesting the
presence of some intact Lp[a] in these extracts. These results suggest that
Lp[a] accumulates preferentially to LDL in plaques, and that plaque apo[a]
is directly associated with plasma apo[a] levels and is in a form that is
less easily removable than most of the apoB. This preferential accumulation
of apo[a] as a tightly bound fraction in lesions, could be responsible for
the independent association of Lp[a] with cardiovascular disease in humans.
ARTICLES
Quantification of apo[a] and apoB in human atherosclerotic lesions
Department of Vascular Cell Biology and Atherosclerosis Research, Research Institute, Cleveland Clinic Foundation, OH 44195.
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