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A more recent version of this article appeared on March 1, 2008

Papers In Press, published online ahead of print November 21, 2007
J. Lipid Res., doi:10.1194/jlr.M700329-JLR200
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Submitted on July 19, 2007
Revised on November 21, 2007
Accepted on November 21, 2007

Angiotensin II increases vascular proteoglycan content preceding and contributing to atherosclerosis development

Fei Huang, Joel C. Thompson, Patricia G. Wilson, Hnin H. Aung, John C. Rutledge, and Lisa R. Tannock

Internal Medicine, University of Kentucky, Lexington, KY 40536-0200

Corresponding Author: Lisa.Tannock{at}uky.edu

Angiotensin II (angII) is known to promote atherosclerosis; however, the mechanisms involved are not fully understood. To determine if angII stimulates proteoglycan production and LDL retention, LDL receptor-deficient (LDLR-/-) mice were infused with angII (1000 ng/kg/min) or saline via osmotic minipumps. To control for the hypertensive effect of angII a parallel group received norepinephrine (NE; 5.6 mg/kg/d). Arterial lipid accumulation was evaluated by measuring the retention rate of LDL in isolated carotid arteries perfused ex vivo. Mice infused with angII had increased vascular content of biglycan and perlecan, and retained twice as much LDL as saline or NE infused mice, although no group developed atherosclerosis at this time. To determine if this increase in biglycan and perlecan content predisposed to atherosclerosis development, mice were infused with angII, saline or NE for 4 weeks, then pumps were removed and mice received an atherogenic Western diet for a further 6 weeks. Mice that had received angII infusions had 3-fold increased atherosclerosis compared to mice that had received saline or NE, and apoB co-localized with both proteoglycans. Thus, one mechanism by which angII promotes atherosclerosis is increased proteoglycan synthesis and increased arterial LDL retention, which precedes and contributes to atherosclerosis development.


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[Abstract] [Full Text] [PDF]


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