Smith E B, Cochran S
University of Aberdeen Department of Clinical Biochemistry, Aberdeen Royal Infirmary, Foresterhill, Scotland, U.K.
Atherosclerosis. 1990 Oct;84(2-3):173-81. doi: 10.1016/0021-9150(90)90088-z.
The extracellular lipid that accumulates in fibrous atherosclerotic lesions appears to be derived directly from plasma low density lipoprotein (LDL). One factor that may influence the lipid deposition is immobilization of part of the LDL in lesions, and an immobilized fraction can be released by incubation with the fibrinolytic enzyme, plasmin, suggesting that it is associated with fibrin. The lipoprotein variant Lp(a) is associated with increased risk of arterial disease, and its characteristic apoprotein, apo(a), is structurally related to plasminogen, suggesting that it might bind to the plasminogen binding sites on fibrin. In this study we have compared blood Lp(a) and the soluble and plasmin-releasable Lp(a) in 45 samples of normal intima and different types of lesion. Levels of soluble and plasmin-releasable Lp(a) were dependent on both blood level and type of tissue sample. Although the amount of soluble LDL was 5-20 times higher than Lp(a) in intima, the amounts released by plasmin were similar, and Lp(a) appears to account for most of the apo B-containing lipoprotein that is immobilized in lesions.
