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

  • Vignesh Murugesan
  • Eva Degerman
  • Anki Knutsson
  • Pontus Dunér
  • Ann-Kristin Holmén-Pålbrink
  • Anna Hultgårdh
  • Uwe Rauch
Publishing year: 2017-07-29
Language: English
Pages: 235-245
Publication/Series: Journal of Vascular Research
Volume: 54
Document type: Journal article
Publisher: Karger

Abstract english

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.


  • Cardiac and Cardiovascular Systems


  • Vessel Wall Biology
  • Insulin Signal Transduction
  • Experimental Cardiovascular Research Unit
  • ISSN: 1423-0135
E-mail: ann-kristin [dot] holmen-palbrink [at] med [dot] lu [dot] se

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