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Expression of the lyst(beige) mutation is atheroprotective in chow-fed apolipoprotein e-deficient mice

Academic Article
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Overview

authors

  • Petrovan, R. J.
  • Yuan, Y.
  • Curtiss, Linda

publication date

  • February 2008

journal

  • Journal of Lipid Research  Journal

abstract

  • Lyst(beige) mice crossed with hyperlipidemic low density lipoprotein receptor-deficient mice (BgLDLr(-/-)) display increased lesion area and a more stable lesion morphology. To verify that the beige phenotype is not unique to LDLr(-/-) mice, we examined atherosclerosis in beige, apolipoprotein E-deficient mutant mice (BgApoE(-/-)). Severe diet-induced hyperlipidemia in BgApoE(-/-) mice resulted in increased aortic sinus lesion areas compared with controls. Minimal aortic lesions were observed in both genotypes on a chow diet. Nevertheless, BgApoE(-/-) mice displayed drastically reduced aortic sinus lesion growth. Reconstitution with bone marrow (BM) from green fluorescent protein mice created chimeric animals that allowed for the identification of donor-derived cells within lesions. Expressing the beige mutation exclusively in BM-derived cells had no impact on plaque development, yet the beige mutation in all cells except the BM-derived cells led to significantly larger aortic sinus lesion areas. Both mRNA and secreted protein levels of monocyte chemoattractant protein 1 were altered in quiescent and phorbol ester-stimulated cultured macrophages, vascular smooth muscle cells, and aortic endothelial cells isolated from BgApoE(-/-) mice. Thus, expression of the beige mutation in all cell types involved in lesion development contributed to atheroprotection in chow-fed ApoE(-/-) mice.

subject areas

  • Animal Feed
  • Animals
  • Apolipoproteins E
  • Atherosclerosis
  • Dietary Fats
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mutation
  • Proteins
  • Receptors, LDL
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Research

keywords

  • bone marrow transplantation
  • low density lipoprotein receptor-deficient mice
  • macrophage
  • plaque
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Identity

International Standard Serial Number (ISSN)

  • 0022-2275

Digital Object Identifier (DOI)

  • 10.1194/jlr.M700410-JLR200

PubMed ID

  • 17982137
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Additional Document Info

start page

  • 429

end page

  • 437

volume

  • 49

issue

  • 2

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