Abstract
Experimental and clinical data indicate that the initiation and progress of atherosclerosis and its clinical manifestations are first caused by circulating apoB-100 lipoproteins that enter and are retained in the arterial intima. Extracellular sulfated proteoglycans (PGs) of the intima are the retention agents. The PGs also initiate physical and biochemical lipoprotein degradation with the production of bioactive, lipid products that trigger an inflammatory response that leads to atherosclerosis. There are many simple methods for measuring abnormalities of circulating lipoproteins and their relation to atherosclerotic cardiovascular disease (ACVD). However, limited research aims to evaluate procedures that could report quantitatively about the contribution of the interaction of apoB-100 lipoprotein-arterial intima PGs to clinical manifestation of ACVD. In the present review we discuss observations indicating that simple ex vivo evaluation of the affinity of apoB-100 lipoproteins for arterial PGs and glycosaminoglycans (GAGs) can give an indication of its association with clinical manifestations of atherosclerosis. In addition, we discuss molecular and cellular aspects of the apoB-100 lipoproteins association with arterial PGs that are related to atherogenesis and that support the experimental framework behind the current “Response-to-Retention” hypothesis of atherosclerosis.
Highlights
The deposition of cholesterol-containing apoB-100 lipoproteins in the extracellular arterial intima is a critical initial step in the development of atherosclerotic lesions
A recent consensus document reviewed the evidence that connects the levels of circulating apoB-100 lipoproteins, and their interaction with the intima and the clinical events caused by atherosclerosis [1]
Garces et al [15] explored this observation in a study in which low density lipoproteins (LDL)-PG affinity was measured in subjects with obesity but not type 2 diabetes (T2D), in subjects with obesity with TD2, in subjects with T2D but no diabetes and in apparently healthy controls with no obesity or T2D The results showed that obesity, with or without T2D, was associated with significantly higher values of plasma LDL-PG precipitation (18 μg LDL cholesterol (LDL-C) precipitated/mg apoB added) compared to 11.7 μg of LDL-C precipitated/mg apoB added in subjects with no obesity
Summary
The deposition of cholesterol-containing apoB-100 lipoproteins in the extracellular arterial intima is a critical initial step in the development of atherosclerotic lesions. We discuss the results of studies aimed to evaluate whether the affinity of LDL in plasma or serum for arterial PGs were associated with clinical manifestations of the risk for ACVD.
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