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European Heart Journal 1990 11(Supplement E):158-167; doi:10.1093/eurheartj/11.suppl_E.158
Copyright © 1990 by the European Society of Cardiology.
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© 1990 The European Society of Cardiology

Transfer of lipoproteins from plasma to the cell populations of the normal and atherosclerotic arterial tissue

G. Bondjers, O. Wiklund, G. Fager, E. H. Camejo and G. Camejo

Wallenberg Laboratory for Cardiovascular Research, University of Göteborg Göteborg, Sweden

Address for correspondence: Göran Bondjers, Wallenberg Laboratory for Cardiovascular Research, Sahlgrenska sjukhuset, S-413 45 Göteborg, Sweden

It appears that retention of lipoproteins rather than increased influx is the basis for lipoprotein deposition in arterial tissue during atherogenesis. Binding of lipoproteins to arterial proteoglycans is mediated by a peptide sequence considered to be involved in the interaction between the lipoproteins and the lipoprotein receptor. Consequently, in the presence of an excess of arterial proteoglycan, receptor-mediated cellular uptake of LDL is inhibited. However, LDL which has been precipitated by proteoglycan and subsequently resolubilized is taken up more avidly than native LDL, both in rnacrophages and in smooth muscle cells. This appears to be due to selection by the proteoglycans of a more reactive fraction of LDL. This fraction has a smaller molecular size and less surface phospholipids. As smaller LDL particles also have a higher transfer rate into the arterial tissue they may be particularly atherogenic. Low density lipoproteins appear to be taken up with higher affnity by arterial macrophages than by smooth muscle cells. The selective transfer of the LDL to macrophages can be inhibited by {alpha}-tocopherol, suggesting that oxidative modification may be involved in this process. The role of foam cells in atherogenesis is discussed in the context of the energy requirements of the arterial wall.

Key Words: Arterial proteoglycans • lipoproteins • lipoprotein receptor


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