Increased atherosclerosis in mice with increased vascular biglycan content.

Abstract:

OBJECTIVE:The response to retention hypothesis of atherogenesis proposes that atherosclerosis is initiated via the retention of atherogenic lipoproteins by vascular proteoglycans. Co-localization studies suggest that of all the vascular proteoglycans, biglycan is the one most closely co-localized with LDL. The goal of this study was to determine if over-expression of biglycan in hyperlipidemic mice would increase atherosclerosis development. METHODS:Transgenic mice were developed by expressing biglycan under control of the smooth muscle actin promoter, and were crossed to the LDL receptor deficient (C57BL/6 background) atherosclerotic mouse model. Biglycan transgenic and non-transgenic control mice were fed an atherogenic Western diet for 4-12 weeks. RESULTS:LDL receptor deficient mice overexpressing biglycan under control of the smooth muscle alpha actin promoter had increased atherosclerosis development that correlated with vascular biglycan content. CONCLUSION:Increased vascular biglycan content predisposes to increased lipid retention and increased atherosclerosis development.

journal_name

Atherosclerosis

journal_title

Atherosclerosis

authors

Thompson JC,Tang T,Wilson PG,Yoder MH,Tannock LR

doi

10.1016/j.atherosclerosis.2014.03.037

subject

Has Abstract

pub_date

2014-07-01 00:00:00

pages

71-5

issue

1

eissn

0021-9150

issn

1879-1484

pii

S0021-9150(14)00201-9

journal_volume

235

pub_type

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