Thompson Publishes Findings About Increased Atherosclerosis in Mice

Increased atherosclerosis in mice with increased vascular biglycan content. Thompson JC, Tang T, Wilson PG, Yoder MH, Tannock LR. Atherosclerosis. 2014 Apr 15;235(1):71-75. doi: 10.1016/j.atherosclerosis.2014.03.037. [Epub] PMID: 24816040

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.