Cited by 45Proteoglycans and glycosaminoglycans researchAtherosclerosis and Cardiovascular DiseasesCholesterol and Lipid Metabolism

Increased atherosclerosis in mice with increased vascular biglycan content

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Thompson, Joel C., Tang, Tao, Wilson, Patricia G., Yoder, Meghan H., Tannock, Lisa R.·2014·Atherosclerosis

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.

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Crossref · 10.1016/j.atherosclerosis.2014.03.037

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  • Transgenic mice over-expressing biglycan in VSMCs show more lipid retention and increased atherosclerosis than wild-type litter-mates.

    “Transgenic mice over-expressing biglycan in VSMCs show more lipid retention and increased atherosclerosis than wild-type litter-mates 114 .”

    From Vascular smooth muscle cells in atherosclerosis (2019) · cites this paper as [114]

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  1. [16]Schwenke DC Carew TE Initiation of atherosclerotic lesions in cholesterol-fed rabbits Arteriosclerosis 1989 9 908 918 2590068
  2. [24]Wilson PG Thompson JC Webb NR SAA, but not CRP, stimulates vascular proteoglycan synthesis in a pro-atherogenic manner Am J Pathol 2008 173 1902 1910 18974302 PMC2626400

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Authors
Thompson, J. C., Tang, T., Wilson, P. G., Yoder, M. H., & Tannock, L. R.
Affiliations
  • University of Kentucky (US)
  • United States Department of Veterans Affairs (US)
Corresponding author
Tannock, Lisa R.
Venue
Atherosclerosis
Publisher
Elsevier BV
Published
2014-07
Volume
235
Issue
1
Pages
71-75
ISSN
0021-9150 (ISSN-L)
OpenAlex
W2016360431
Cited by
45
References
28
Citations by year
2026: 2 · 2025: 2 · 2024: 5 · 2023: 4 · 2021: 5 · 2020: 3 · 2019: 5 · 2018: 5 · 2017: 3 · 2016: 3 · 2015: 3 · 2014: 5
FWCI
2.32
Type
journal article
Language
en
Open access
Locations
  • Atherosclerosis (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Heart, Lung and Blood Institute of the National Institutes of Health (RO1HL082772, RO1HL082772-0351)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Proteoglycans and glycosaminoglycans research
  • Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
  • Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
Keywords
biglycan, LDL receptor deficiency, hyperlipidemia, Western diet, transgenic mice, lipid retention
MeSH terms
Actins, Animals, Blood Vessels, Disease Models, Animal, Female, Hyperlipidemias, Male, Mice, Inbred C57BL, Mice, Transgenic, Promoter Regions, Genetic, Proteoglycans, Transgenes, Atherosclerosis, Mice, Biglycan

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