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Increased atherosclerosis in mice with increased vascular biglycan content
Joel C Thompson1, Tao Tang1, Patricia G Wilson1
1Division of Endocrinology and Molecular Medicine, Saha Cardiovascular Research Center, University of Kentucky, Lexington, KY, USA.
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.
