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.
|Number of pages||5|
|State||Published - Jul 2014|
Bibliographical noteFunding Information:
Research reported in this study was supported by the National Heart, Lung and Blood Institute of the National Institutes of Health under award number RO1HL082772 and RO1HL082772-0351 , both to LRT, and an award from the American Heart Association, Great Rivers Affiliate to JCT. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health or the American Heart Association.
- LDL retention
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine