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Journal of Lipid Research, Vol 33, 1315-1325, Copyright © 1992 by Lipid Research, Inc.
YB de Rijke, G Jurgens, EM Hessels, A Hermann and TJ van Berkel
High levels of Lp[a] in blood form an independent risk factor for
atherosclerosis. Oxidative modification of Lp[a] may be involved in the
suggested atherogenic action of Lp[a]. After Cu(2+)-mediated oxidative
modification of the 440 kDa and 610 kDa apo[a] isoforms of lipoprotein[a]
(Ox-Lp[a]), the in vivo fate was investigated in rats. Ox-Lp[a], when
injected into rats, was rapidly removed from the blood circulation by the
liver, in which the intrahepatic fate is dependent on the degree of
oxidation of the isoforms. Upon oxidation to a slightly increased negative
charge of Lp[a], the high molecular weight form of Lp[a] is recognized more
efficiently by the Kupffer cells than by the endothelial cells. When the
liver uptake of Ox-Lp[a] is blocked by preinjection of polyinosinic acid
(poly I), the association of Ox- Lp[a] with the rat heart is increased
20-fold. In vitro studies show that the association and degradation of
125I-labeled Ox-Lp[a] with liver endothelial and Kupffer cells was
inhibited by oxidized LDL (Ox- LDL), poly I, or Ox-Lp[a] itself by 60-90%,
while only a partial competition was found with acetylated-LDL (up to 25%).
In conclusion, after oxidative modification of Lp[a], there is recognition
of Ox-Lp[a] by specific oxidized-lipoprotein receptors on liver endothelial
and Kupffer cells; the relative importance at low degrees of oxidation of
Lp[a] is dependent on the molecular weight of the apo[a] isoforms. Under
conditions in which liver uptake is not adequate, the deposition of
Ox-Lp[a] in the heart may be of potential pathological importance.
ARTICLES
In vivo fate and scavenger receptor recognition of oxidized lipoprotein[a] isoforms in rats
Division of Biopharmaceutics, Sylvius Laboratory, University of Leiden, The Netherlands.
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