Journal
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
Volume 22, Issue 3, Pages 462-468Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/hq0302.105378
Keywords
apoE deficiency; LDL receptor deficiency; atherosclerosis; proteoglycans; apolipoproteins
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Funding
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL052848] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [K11DK002345] Funding Source: NIH RePORTER
- NHLBI NIH HHS [HL-02788, HL-52848] Funding Source: Medline
- NIDDK NIH HHS [DK-02345] Funding Source: Medline
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Proteoglycan accumulation within the arterial intima has been implicated in lipoprotein retention and in atherosclerosis progression in humans. Two commonly studied murine models of atherosclerosis, the apolipoprotein E (apoE)-deficient (apoE-/-) mouse and the low density lipoprotein receptor-deficient (LDLR-/-) mouse, develop arterial lesions similar to those of human atherosclerosis. However, specific proteoglycan classes that accumulate in lesions of these mice and their relation to the retention of specific apolipoproteins have not been previously determined. In this report, we characterized the distribution of proteoglycans (versican, biglycan, and perlecan) and apolipoproteins (apoB, apoA-1, and apoE) in proximal aortic lesions of chow-fed apoE-/- and LDLR -/- mice at 10, 52, and 73 weeks of age. We observed that similar to the apoE-/- mice, the LDLR-/- mice develop intermediate and advanced plaques within 52 weeks of age. Perlecan and biglycan (both are proteoglycans) appeared early in lesion development with distinct expression patterns as the plaques advanced. Versican, a major proteoglycan detected in human plaques, was mostly absent in both strains. ApoA-I and apoB were detected in early through advanced lesions in regions of proteoglycan accumulation in both strains. Our results indicate that proteoglycans may contribute to the retention of lipoproteins at the earliest stage of atherosclerosis in murine models of atherosclerosis.
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