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Vol. 42, No. 6, 2005
Issue release date: November–December 2005
Section title: Research Paper
J Vasc Res 2005;42:492–502
(DOI:10.1159/000088139)

Broad-Spectrum Chemokine Inhibition Reduces Vascular Macrophage Accumulation and Collagenolysis Consistent with Plaque Stabilization in Mice

Reckless J.a · Tatalick L.b · Wilbert S.b · McKilligin E.a · Grainger D.J.a
aDepartment of Medicine, University of Cambridge, Addenbrooke’s Hospital, Cambridge, UK; bNeoRx Corporation, Seattle, Wash., USA

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Article / Publication Details

First-Page Preview
Abstract of Research Paper

Received: 2/28/2005
Accepted: 6/25/2005
Published online: 10/20/2005
Issue release date: November–December 2005

Number of Print Pages: 11
Number of Figures: 5
Number of Tables: 0

ISSN: 1018-1172 (Print)
eISSN: 1423-0135 (Online)

For additional information: http://www.karger.com/JVR

Abstract

Background: A major determinant of the risk of myocardial infarction is the stability of the atherosclerotic plaque. Macrophage-rich plaques are more vulnerable to rupture, since macrophages excrete an excess of matrix-degrading enzymes over their inhibitors, reducing collagen content and thinning the fibrous cap. Several genetic studies have shown that disruption of signalling by the chemokine monocyte chemoattractant protein 1 reduced the lipid lesion area and macrophage accumulation in the vessel wall. Methods: We have tested whether a similar reduction in macrophage accumulation could be achieved pharmacologically by treating apolipoprotein-E-deficient mice with the chemokine inhibitor NR58-3.14.3. Results: Mice treated for various periods of time (from several days to 6 months) with NR58-3.14.3 (approximately 30 mg/kg/day) consistently had 30–40% fewer macrophages in vascular lesions, compared with mice treated with the inactive control NR58-3.14.4 or PBS vehicle. Similarly, cleaved collagen staining was lower in mice treated for up to 7 days, although this effect was not maintained when treatment time was extended to 12 weeks. The vascular lipid lesion area was unaffected by treatment, but total collagen I staining and smooth muscle cell number were both increased, suggesting that a shift to a more stable plaque phenotype had been achieved. Conclusions: Strategies, such as chemokine inhibition, to attenuate macrophage accumulation may therefore be useful to promote stabilization of atherosclerotic plaques.

© 2005 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Research Paper

Received: 2/28/2005
Accepted: 6/25/2005
Published online: 10/20/2005
Issue release date: November–December 2005

Number of Print Pages: 11
Number of Figures: 5
Number of Tables: 0

ISSN: 1018-1172 (Print)
eISSN: 1423-0135 (Online)

For additional information: http://www.karger.com/JVR


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