Article

 

Deficiency of CCAAT/Enhancer Binding Protein-Epsilon Reduces Atherosclerotic Lesions in LDLR-/- Mice 公开 Deposited

可下载的内容

下载PDF文件
https://ir.library.oregonstate.edu/concern/articles/9593tw85t

Descriptions

Attribute NameValues
Creator
Abstract
  • The CCAAT/enhancer binding proteins (C/EBPs) are transcription factors involved in hematopoietic cell development and induction of several inflammatory mediators. C/EBPε is expressed only in myeloid cells including monocytes/macrophages. Atherosclerosis is an inflammatory disorder of the vascular wall and circulating immune cells such as monocytes/macrophages. Mice deficient in the low density lipoprotein (LDL) receptor (Ldlr-/-) fed on a high cholesterol diet (HCD) show elevated blood cholesterol levels and are widely used as models to study human atherosclerosis. In this study, we generated Ldlr and Cebpe double-knockout (llee) mice and compared their atherogenic phenotypes to Ldlr single deficient (llEE) mice after HCD. Macrophages from llee mice have reduced lipid uptake by foam cells and impaired phagokinetic motility in vitro compared to macrophages from llEE mice. Also, compared to llEE mice, llee mice have alterations of lipid metabolism, and reduced atheroma and obesity, particularly the males. Peritoneal macrophages of llee male mice have reduced mRNA expression of FABP4, a fatty acid binding protein implicated in atherosclerosis. Overall, our study suggests that the myeloid specific factor C/EBPε is involved in systemic lipid metabolism and that silencing of C/EBPε could decrease the development of atherosclerosis.
Resource Type
DOI
Date Available
Date Issued
Citation
  • Okamoto R, Gery S, Gombart AF, Wang X, Castellani LW, et al. (2014) Deficiency of CCAAT/Enhancer Binding Protein-Epsilon Reduces Atherosclerotic Lesions in LDLR-/- Mice. PLoS ONE 9(1): e85341. doi:10.1371/journal.pone.0085341
Journal Title
Journal Volume
  • 9
Journal Issue/Number
  • 1
权利声明
Funding Statement (additional comments about funding)
  • This work was supported by National Institutes of Health (NIH) grants (2R01 CA026038-32, 5R01AI65604-6), SWLF, the Tom Collier Memorial RegattaFoundation, Parker Hughes Fund, East Meets West Cedars-Sinai Fund, as well as, A*STAR of Singapore.
Publisher
Peer Reviewed
Language
Replaces

关联

Parents:

This work has no parents.

单件