Accumulation of 125I-tyramine cellobiose-labeled low density lipoprotein is greater in the atherosclerosis-susceptible region of White Carneau pigeon aorta and further enhanced once atherosclerotic lesions develop.

Abstract

Previous studies have suggested that greater arterial concentrations of undegraded low density lipoprotein (LDL) and/or greater arterial rates of LDL degradation may play role(s) in determining regional differences in arterial susceptibility to atherosclerosis in rabbits (Schwenke and Carew, Arteriosclerosis 1989;9:895-918). The White Carneau (WC) pigeon is also useful for investigating potential mechanism(s) that might account for regional variation in arterial susceptibility to atherosclerosis because atherosclerosis develops predictably in the aorta at the level of the cellac bifurcation (atherosclerosis-susceptible celiac site). In this study we sought to determine whether the 123 I-tyramine cellobiose (

An Update of the Grützbalgϕ Hypothesis: The Role of Thrombosis and Coagulation in Atherosclerotic Progression

“…Different studies focused on the entry of macrophages into the intima, the formation of foam cells from macrophages, the physical transport properties for lipoproteins, or lipid metabolism in the different layers of the wall. Most studies suggested that the major role of arterial intima was as a passive trap for lipoproteins (5)(6)(7)(8)(9). Intriguingly for this review, these studies also suggested that the intima trapped fibrinogen and other coagulation factors simply by molecular sizing (10)(11)(12).…”

Artery regional properties and atherosclerosis susceptibility

“…Thus, cell to matrix ratios at the atherosclerosis-prone site were distinctly different in WC and SR celiac bifurcation sites. WC pigeons typically had increased matrix materials which potentially serve to trap and retain plasma low density lipoprotein (LDL) (Schwenke and St. Clair, 1992). A number of studies have been published demonstrating increased proteoglycan content at atherosclerosis-prone sites of pigeons (Curwen and Smith, 1977) and in human atherosclerotic lesions (Stary et al, 1995).…”

Cholesterol efflux is defective in macrophages from atherosclerosis-susceptible White Carneau pigeons relative to resistant show racer pigeons.

“…We also know that plasma lipoproteins normally pass into and out of the arterial wall and accumulate in higher concentrations at sites that are susceptible to atherosclerosis. 43 Since pigeon macrophages are attracted to these sites by chemotactic factors, 44 they may come in contact with high concentrations of lipoproteins in the arterial wall. The macrophages could take up some of these plasma lipoproteins, or in more-advanced atherosclerotic plaques, even lipidrich extracellular debris from dead cells could be taken up by phagocytosis, resulting in a high rate of cholesterol input to the cells.…”