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Träfflista för sökning "WFRF:(Rauch Uwe) ;mspu:(article);pers:(Dunér Pontus)"

Search: WFRF:(Rauch Uwe) > Journal article > Dunér Pontus

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  • Murugesan, Vignesh, et al. (author)
  • β-Sarcoglycan Deficiency Reduces Atherosclerotic Plaque Development in ApoE-Null Mice
  • 2017
  • In: Journal of Vascular Research. - : S. Karger AG. - 1423-0135 .- 1018-1172. ; 54, s. 235-245
  • Journal article (peer-reviewed)abstract
    • Background: Smooth muscle cells are important for atheroscleroticplaque stability. Their proper ability to communicatewith the extracellular matrix is crucial for maintainingthe correct tissue integrity. In this study, we have investigatedthe role of β-sarcoglycan within the matrix-binding dystrophin-glycoproteincomplex in the development of atherosclerosis.Results: Atherosclerotic plaque developmentwas significantly reduced in ApoE-deficient mice lackingβ-sarcoglycan, and their plaques contained an increase indifferentiated smooth muscle cells. ApoE-deficient micelacking β-sarcoglycan showed a reduction in ovarian adiposetissue and adipocyte size, while the total weight of theanimals was not significantly different. Western blot analysisof adipose tissues showed a decreased activation of proteinkinase B, while that of AMP-activated kinase was increasedin mice lacking β-sarcoglycan. Analysis of plasma in β-sarcoglycan-deficientmice revealed reduced levels of leptin,adiponectin, insulin, cholesterol, and triglycerides but in-creased levels of IL-6, IL-17, and TNF-α. Conclusions: Our resultsindicate that the dystrophin-glycoprotein complex andβ-sarcoglycan can affect the atherosclerotic process. Furthermore,the results show the effects of β-sarcoglycan deficiencyon adipose tissue and lipid metabolism, which mayalso have contributed to the atherosclerotic plaque reduction.
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2.
  • Shami, Annelie, et al. (author)
  • Dystrophin deficiency reduces atherosclerotic plaque development in ApoE-null mice.
  • 2015
  • In: Scientific Reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 5
  • Journal article (peer-reviewed)abstract
    • Dystrophin of the dystrophin-glycoprotein complex connects the actin cytoskeleton to basement membranes and loss of dystrophin results in Duchenne muscular dystrophy. We have previously shown injury-induced neointima formation of the carotid artery in mice with the mdx mutation (causing dystrophin deficiency) to be increased. To investigate the role of dystrophin in intimal recruitment of smooth muscle cells (SMCs) that maintains plaque stability in atherosclerosis we applied a shear stress-modifying cast around the carotid artery of apolipoprotein E (ApoE)-null mice with and without the mdx mutation. The cast induces formation of atherosclerotic plaques of inflammatory and SMC-rich/fibrous phenotypes in regions of low and oscillatory shear stress, respectively. Unexpectedly, presence of the mdx mutation markedly reduced the development of the inflammatory low shear stress plaques. Further characterization of the low shear stress plaques in ApoE-null mdx mice demonstrated reduced infiltration of CD3(+) T cells, less laminin and a higher SMC content. ApoE-null mdx mice were also found to have a reduced fraction of CD3(+) T cells in the spleen and lower levels of cytokines and monocytes in the circulation. The present study is the first to demonstrate a role for dystrophin in atherosclerosis and unexpectedly shows that this primarily involves immune cells.
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Type of publication
Type of content
peer-reviewed (2)
Author/Editor
Hultgårdh, Anna (2)
Rauch, Uwe (2)
Knutsson, Anki (2)
Murugesan, Vignesh (2)
Degerman, Eva (1)
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Nilsson, Jan (1)
Durbeej-Hjalt, Madel ... (1)
Goncalves, Isabel (1)
Tengryd, Christoffer (1)
Bengtsson, Eva (1)
Shami, Annelie (1)
Holmén-Pålbrink, Ann ... (1)
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University
Lund University (2)
Language
English (2)
Research subject (UKÄ/SCB)
Medical and Health Sciences (2)

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