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
Atherosclerosisjournal_title
Atherosclerosisauthors
Thompson JC,Tang T,Wilson PG,Yoder MH,Tannock LRdoi
10.1016/j.atherosclerosis.2014.03.037subject
Has Abstractpub_date
2014-07-01 00:00:00pages
71-5issue
1eissn
0021-9150issn
1879-1484pii
S0021-9150(14)00201-9journal_volume
235pub_type
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