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β-Sarcoglycan Deficiency Reduces Atherosclerotic Plaque Development in ApoE-Null Mice

Murugesan, Vignesh LU ; Degerman, Eva LU ; Knutsson, Anki LU ; Dunér, Pontus LU ; Holmén-Pålbrink, Ann-Kristin LU ; Hultgårdh, Anna LU and Rauch, Uwe LU (2017) In Journal of Vascular Research1992-01-01+01:00 54. p.235-245
Abstract
Background: Smooth muscle cells are important for atherosclerotic
plaque stability. Their proper ability to communicate
with the extracellular matrix is crucial for maintaining
the correct tissue integrity. In this study, we have investigated
the role of β-sarcoglycan within the matrix-binding dystrophin-glycoprotein
complex in the development of atherosclerosis.
Results: Atherosclerotic plaque development
was significantly reduced in ApoE-deficient mice lacking
β-sarcoglycan, and their plaques contained an increase in
differentiated smooth muscle cells. ApoE-deficient mice
lacking β-sarcoglycan showed a reduction in ovarian adipose
tissue and adipocyte size, while the total weight of... (More)
Background: Smooth muscle cells are important for atherosclerotic
plaque stability. Their proper ability to communicate
with the extracellular matrix is crucial for maintaining
the correct tissue integrity. In this study, we have investigated
the role of β-sarcoglycan within the matrix-binding dystrophin-glycoprotein
complex in the development of atherosclerosis.
Results: Atherosclerotic plaque development
was significantly reduced in ApoE-deficient mice lacking
β-sarcoglycan, and their plaques contained an increase in
differentiated smooth muscle cells. ApoE-deficient mice
lacking β-sarcoglycan showed a reduction in ovarian adipose
tissue and adipocyte size, while the total weight of the
animals was not significantly different. Western blot analysis
of adipose tissues showed a decreased activation of protein
kinase B, while that of AMP-activated kinase was increased
in mice lacking β-sarcoglycan. Analysis of plasma in β-sarcoglycan-deficient
mice revealed reduced levels of leptin,
adiponectin, insulin, cholesterol, and triglycerides but in-
creased levels of IL-6, IL-17, and TNF-α. Conclusions: Our results
indicate that the dystrophin-glycoprotein complex and
β-sarcoglycan can affect the atherosclerotic process. Furthermore,
the results show the effects of β-sarcoglycan deficiency
on adipose tissue and lipid metabolism, which may
also have contributed to the atherosclerotic plaque reduction.
(Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Journal of Vascular Research1992-01-01+01:00
volume
54
pages
235 - 245
publisher
Karger
external identifiers
  • scopus:85026883705
  • wos:000409104300006
ISSN
1423-0135
DOI
10.1159/000478014
language
English
LU publication?
yes
id
826377a7-0830-4766-b0e4-658da50847be
date added to LUP
2017-08-11 16:59:51
date last changed
2018-01-16 13:22:43
@article{826377a7-0830-4766-b0e4-658da50847be,
  abstract     = {Background: Smooth muscle cells are important for atherosclerotic<br/>plaque stability. Their proper ability to communicate<br/>with the extracellular matrix is crucial for maintaining<br/>the correct tissue integrity. In this study, we have investigated<br/>the role of β-sarcoglycan within the matrix-binding dystrophin-glycoprotein<br/>complex in the development of atherosclerosis.<br/>Results: Atherosclerotic plaque development<br/>was significantly reduced in ApoE-deficient mice lacking<br/>β-sarcoglycan, and their plaques contained an increase in<br/>differentiated smooth muscle cells. ApoE-deficient mice<br/>lacking β-sarcoglycan showed a reduction in ovarian adipose<br/>tissue and adipocyte size, while the total weight of the<br/>animals was not significantly different. Western blot analysis<br/>of adipose tissues showed a decreased activation of protein<br/>kinase B, while that of AMP-activated kinase was increased<br/>in mice lacking β-sarcoglycan. Analysis of plasma in β-sarcoglycan-deficient<br/>mice revealed reduced levels of leptin,<br/>adiponectin, insulin, cholesterol, and triglycerides but in-<br/>creased levels of IL-6, IL-17, and TNF-α. Conclusions: Our results<br/>indicate that the dystrophin-glycoprotein complex and<br/>β-sarcoglycan can affect the atherosclerotic process. Furthermore,<br/>the results show the effects of β-sarcoglycan deficiency<br/>on adipose tissue and lipid metabolism, which may<br/>also have contributed to the atherosclerotic plaque reduction.<br/>},
  author       = {Murugesan, Vignesh and Degerman, Eva and Knutsson, Anki and Dunér, Pontus and Holmén-Pålbrink, Ann-Kristin and Hultgårdh, Anna and Rauch, Uwe},
  issn         = {1423-0135},
  language     = {eng},
  month        = {07},
  pages        = {235--245},
  publisher    = {Karger},
  series       = {Journal of Vascular Research1992-01-01+01:00},
  title        = {β-Sarcoglycan Deficiency Reduces Atherosclerotic Plaque Development in ApoE-Null Mice},
  url          = {http://dx.doi.org/10.1159/000478014},
  volume       = {54},
  year         = {2017},
}