title: Increased atherosclerosis in mice with increased vascular biglycan content.
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.
  
  
  CONCLUSIONS
  Increased vascular biglycan content predisposes to increased lipid retention and increased atherosclerosis development.
authors.affiliation: Division of Endocrinology and Molecular Medicine, Saha Cardiovascular Research Center, University of Kentucky, Lexington, KY, USA.
authors.forename: Joel C
authors.initials: JC
authors.lastname: Thompson
authors.affiliation: Division of Endocrinology and Molecular Medicine, Saha Cardiovascular Research Center, University of Kentucky, Lexington, KY, USA.
authors.forename: Tao
authors.initials: T
authors.lastname: Tang
authors.affiliation: Division of Endocrinology and Molecular Medicine, Saha Cardiovascular Research Center, University of Kentucky, Lexington, KY, USA.
authors.forename: Patricia G
authors.initials: PG
authors.lastname: Wilson
authors.affiliation: Division of Endocrinology and Molecular Medicine, Saha Cardiovascular Research Center, University of Kentucky, Lexington, KY, USA.
authors.forename: Meghan H
authors.initials: MH
authors.lastname: Yoder
authors.affiliation: Division of Endocrinology and Molecular Medicine, Saha Cardiovascular Research Center, University of Kentucky, Lexington, KY, USA; Department of Veterans Affairs, Lexington, KY, USA. Electronic address: Lisa.Tannock@uky.edu.
authors.forename: Lisa R
authors.initials: LR
authors.lastname: Tannock
mesh_terms: D000199:Actins / Q000235:genetics; D000818:Animals; D050197:Atherosclerosis / Q000378:metabolism* / Q000473:pathology; D058578:Biglycan / Q000378:metabolism*; D001808:Blood Vessels / Q000378:metabolism*; D004195:Disease Models, Animal; D005260:Female; D006949:Hyperlipidemias / Q000378:metabolism / Q000473:pathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D011401:Promoter Regions, Genetic; D011509:Proteoglycans / Q000378:metabolism; D019076:Transgenes
chemical_list: D000199:Actins; D058578:Biglycan; D011509:Proteoglycans
keywords: Atherosclerosis; Biglycan; LDL retention; Mice