J. Lipid Res.
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A more recent version of this article appeared on October 1, 2004

Papers In Press, published online ahead of print July 16, 2004
J. Lipid Res., doi:10.1194/jlr.M400019-JLR200
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Submitted on January 21, 2004
Revised on July 8, 2004
Accepted on July 10, 2004

Atherosclerosis in perlecan heterozygous mice

Reeba K. Vikramadithyan, Yuko Kako, Guangping Chen, Yunying Hu, Eri Arikawa-Hirasawa, Yoshihiko Yamada, and Ira J. Goldberg

Department of Medicine, Columbia University, New York, NY 10032

Corresponding Author: ijg3{at}columbia.edu

The hypothesis that lipoprotein association with perlecan is atherogenic was tested by studying atherosclerosis in mice that had a heterozygous deletion of perlecan, the primary extracellular heparan sulfate proteoglycan in arteries. We first studied the expression of perlecan in mouse lesions and noted that this proteoglycan in aorta was found in the subendothelial matrix. Perlecan was also a major component of the lesional extracellular matrix. Mice with a heterozygous deletion had a reduction in arterial wall perlecan expression. Atherosclerosis in these mice with was studied after crossing the defect onto the apoE and LDL receptor knockout backgrounds. At 12 weeks, chow-fed apoE0 mice with a heterozygous deletion had less atherosclerosis. However, at 24 weeks and in LDL receptor heterozygous background, the presence of a perlecan knockout allele did not significantly alter lesion size. Thus, it appears that loss of perlecan leads to less atherosclerosis in early lesions. While this might be due to a decrease in lipoprotein retention, it should be noted that perlecan might mediate multiple other processes that could, in sum, accelerate atherosclerosis.


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