Increased atherosclerosis in mice with increased vascular biglycan content

Joel C. Thompson; Tao Tang; Patricia G. Wilson; Meghan H. Yoder; Lisa R. Tannock

doi:10.1016/j.atherosclerosis.2014.03.037

Increased atherosclerosis in mice with increased vascular biglycan content

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

Research output: Contribution to journal › Article › peer-review

40 Scopus citations

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.

Original language	English
Pages (from-to)	71-75
Number of pages	5
Journal	Atherosclerosis
Volume	235
Issue number	1
DOIs	https://doi.org/10.1016/j.atherosclerosis.2014.03.037
State	Published - Jul 2014

Bibliographical note

Funding 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.

Keywords

Atherosclerosis
Biglycan
LDL retention
Mice

ASJC Scopus subject areas

Cardiology and Cardiovascular Medicine

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10.1016/j.atherosclerosis.2014.03.037

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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. Conclusion: Increased vascular biglycan content predisposes to increased lipid retention and increased atherosclerosis development.",

keywords = "Atherosclerosis, Biglycan, LDL retention, Mice",

author = "Thompson, {Joel C.} and Tao Tang and Wilson, {Patricia G.} and Yoder, {Meghan H.} and Tannock, {Lisa R.}",

note = "Funding 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.",

year = "2014",

month = jul,

doi = "10.1016/j.atherosclerosis.2014.03.037",

language = "English",

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AU - Thompson, Joel C.

AU - Tang, Tao

AU - Wilson, Patricia G.

AU - Yoder, Meghan H.

AU - Tannock, Lisa R.

N1 - Funding 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.

PY - 2014/7

Y1 - 2014/7

N2 - 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.

AB - 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.

KW - Atherosclerosis

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KW - LDL retention

KW - Mice

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Increased atherosclerosis in mice with increased vascular biglycan content

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

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