Submitted on December 19, 2002
Revised on January 16, 2003
Accepted on January 7, 2003
Effect of fluid mechanical stresses and plasma constituents on aggregation of lowdensity lipoprotein
Roy M. Talbot, Jessica D. del Rio, and Peter D. Weinberg
School of Animal and Microbial Sciences, University of Reading, Reading RG6 6AJ
Corresponding Author: p.d.weinberg{at}reading.ac.uk
Abstract Low density lipoprotein (LDL) aggregates when exposed to even moderate fluid mechanical stresses in the laboratory, yet its half-life in the circulation is 2-3 days, implying that little aggregation occurs. LDL may be protected from aggregation in vivo by components of plasma, or by a qualitative difference in flows. Previous studies have shown that high density lipoprotein (HDL) and albumin inhibit the aggregation induced by vortexing. Using a more reproducible method of inducing aggregation, and assessing aggregation both spectrophotometrically and by sedimentation techniques, we showed that at physiological concentrations albumin is the more effective inhibitor, and that aggregation is substantially but not completely inhibited in plasma. Heat-denatured and fatty-acid stripped albumin were more effective inhibitors than normal albumin, supporting the idea that hydrophobic interactions are involved. Aggregation of LDL in a model reproducing several aspects of flow in the circulation was 200-fold slower, but was still inhibited by HDL and albumin, suggesting similar mechanisms are involved. Within the sensitivity of our technique, LDL aggregation did not occur in plasma exposed to these flows. Thus, as a result of the characteristics of blood flow and inhibitory effects of plasma components, particularly albumin, LDL aggregation is unlikely to occur within the circulation.
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