| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
© 1999 American Heart Association, Inc.
Original Contributions |
Focal Increases in Vascular Cell Adhesion Molecule-1 and Intimal Macrophages at Atherosclerosis-Susceptible Sites in the Rabbit Aorta After Short-Term Cholesterol Feeding
From the Department of Biomedical Engineering, Duke University, Durham, NC.
Correspondence to George A. Truskey, Department of Biomedical Engineering, Duke University, 136 Hudson Hall, Box 90281, Durham, NC 27708-0281. E-mail gtruskey{at}acpub.duke.edu
Abstract—We tested the hypotheses that vascular cell adhesion molecule-1 (VCAM-1) expression on endothelium at lesion-prone sites in the rabbit aorta correlates with exposure to plasma cholesterol and that macrophage accumulation is associated with endothelial cells expressing VCAM-1. After rabbits were fed 0.25% cholesterol for 2 weeks, VCAM-1 expression was selectively increased at the distal and lateral portions of the major abdominal branches. In the arch and the celiac, superior mesenteric, and renal artery branches, VCAM-1 expression was positively correlated with the plasma cholesterol integrated over the duration of the experiments. After 2 weeks of cholesterol feeding, more macrophages were present around distal and lateral portions of the intercostal arteries and major abdominal branches relative to nonbranch regions. In the arch and around the intercostals and major abdominal branches, macrophage densities were positively correlated with the integrated plasma cholesterol. VCAM-1 and macrophage levels were correlated in lesion-prone regions. In normocholesterolemic rabbits, 23±4% (mean±SEM) of the macrophages were directly associated with VCAM-1–positive endothelium. After 2 weeks of 0.25% cholesterol feeding, the association increased to 37±4% (P<0.015). Associations were highest around the lateral and distal regions of the major abdominal branches. These results suggest that (1) VCAM-1 expression and intimal macrophage densities are influenced by plasma cholesterol and regional factors such as arterial fluid dynamics and (2) VCAM-1 plays a significant role in the localization of macrophages.
Key Words: atherosclerosis • endothelium • monocyte • hypercholesterolemia
This article has been cited by other articles:
 |
|
 |
|
  A. K. Stannard, R. Khurana, I. M. Evans, V. Sofra, D. I.R. Holmes, and I. Zachary Vascular Endothelial Growth Factor Synergistically Enhances Induction of E-Selectin by Tumor Necrosis Factor-{alpha} Arterioscler Thromb Vasc Biol, March 1, 2007; 27(3): 494 - 502. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. J. Goldschmidt-Clermont, M. A. Creager, D. W. Lorsordo, G. K.W. Lam, M. Wassef, and V. J. Dzau Atherosclerosis 2005: Recent Discoveries and Novel Hypotheses Circulation, November 22, 2005; 112(21): 3348 - 3353. [Full Text] [PDF]
|
|
|
|
|
|
M. Namiki, S. Kawashima, T. Yamashita, M. Ozaki, T. Hirase, T. Ishida, N. Inoue, K.-i. Hirata, A. Matsukawa, R. Morishita, et al. Local Overexpression of Monocyte Chemoattractant Protein-1 at Vessel Wall Induces Infiltration of Macrophages and Formation of Atherosclerotic Lesion: Synergism With Hypercholesterolemia Arterioscler Thromb Vasc Biol, January 1, 2002; 22(1): 115 - 120. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. K. Stannard, D. R. Riddell, S. M. Sacre, A. D. Tagalakis, C. Langer, A. von Eckardstein, P. Cullen, T. Athanasopoulos, G. Dickson, and J. S. Owen Cell-derived Apolipoprotein E (ApoE) Particles Inhibit Vascular Cell Adhesion Molecule-1 (VCAM-1) Expression in Human Endothelial Cells J. Biol. Chem., November 30, 2001; 276(49): 46011 - 46016. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Fruebis, M. Silvestre, D. Shelton, C. Napoli, and W. Palinski Inhibition of VCAM-1 expression in the arterial wall is shared by structurally different antioxidants that reduce early atherosclerosis in NZW rabbits J. Lipid Res., November 1, 1999; 40(11): 1958 - 1966. [Abstract] [Full Text]
|
|