J. Lipid Res.
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A more recent version of this article appeared on September 1, 2005

Papers In Press, published online ahead of print July 1, 2005
J. Lipid Res., doi:10.1194/jlr.M500241-JLR200
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Submitted on June 10, 2005
Accepted on June 27, 2005

Endostatin binds biglycan and LDL and interferes with LDL retention to subendothelial matrix during atherosclerosis

Xiaokun Zeng, Joshua Chen, Yury I. Miller, Kashi Javaherian, and Karen S. Moulton

Vascular Biology Program, Dept of Surgery, Children's Hospital, Boston, MA

Corresponding Author: karen.moulton{at}childrens.harvard.edu

Retention of lipoproteins to proteoglycans in the subendothelial matrix is an early event in atherosclerosis. We recently reported collagen XVIII and its proteolytically-released fragment endostatin are differentially depleted in blood vessels affected by atherosclerosis. Loss of collagen XVIII/endostatin in atherosclerosis-prone mice enhanced plaque neovascularization and increased vascular permeability to lipids by distinct mechanisms. Impaired endothelial barrier function increased the influx of lipoproteins across the endothelium; however, we hypothesized that enhanced retention might be a second mechanism leading to the increased lipid content in atheromas lacking collagen XVIII. We now demonstrate a novel property of endostatin that binds both the matrix proteoglycan biglycan and LDL and interferes with LDL retention to biglycan and to subendothelial matrix. A peptide encompassing the alpha coil in the endostatin crystal structure mediates the major blocking effect of endostatin on LDL retention. Endostatin inhibits macrophage uptake of biglycan-associated LDL indirectly by interfering with LDL retention to biglycan, but it has no direct effect on macrophage uptake of native or modified lipoproteins. Thus, loss of endostatin in advanced atheromas enhances lipoprotein retention in subendothelial matrix. Our data reveals a third protective role of this vascular basement membrane component during atherosclerosis.


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