Accessibility navigation

Effect of fluid mechanical stresses and plasma constituents on aggregation of LDL

Talbot, R. M., del Rio, J. D. and Weinberg, P. D. (2003) Effect of fluid mechanical stresses and plasma constituents on aggregation of LDL. Journal of Lipid Research, 44 (4). pp. 837-845. ISSN 0022-2275

Full text not archived in this repository.

It is advisable to refer to the publisher's version if you intend to cite from this work. See Guidance on citing.

To link to this item DOI: 10.1194/jlr.M200477-JLR200


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 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.jlr Thus, as a result of the characteristics of blood flow and the inhibitory effects of plasma components, particularly albumin, LDL aggregation is unlikely to occur within the circulation.

Item Type:Article
Divisions:Life Sciences > School of Biological Sciences
ID Code:10884
Uncontrolled Keywords:low density lipoprotein self-aggregation, modified low density, lipoprotein, apolipoprotein B-100, hydrophobic interaction, arterial, flow, atherosclerosis, LOW-DENSITY-LIPOPROTEIN, FOAM-CELL-FORMATION, SERUM-ALBUMIN, IN-VITRO, CHOLESTEROL, OXIDATION, INTIMA, RABBIT, ATHEROSCLEROSIS, PHAGOCYTOSIS

University Staff: Request a correction | Centaur Editors: Update this record

Page navigation