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Title: Deficiency of CCAAT/enhancer binding protein-epsilon reduces atherosclerotic lesions in LDLR-/- Mice
Authors: Okamoto, R.
Gery, S.
Gombart, A.F.
Wang, X.
Castellani, L.W.
Akagi, T.
Chen, S.
Arditi, M.
Ho, Q.
Lusis, A.J.
Li, Q.
Koeffler, H.P. 
Issue Date: 28-Jan-2014
Citation: Okamoto, R., Gery, S., Gombart, A.F., Wang, X., Castellani, L.W., Akagi, T., Chen, S., Arditi, M., Ho, Q., Lusis, A.J., Li, Q., Koeffler, H.P. (2014-01-28). Deficiency of CCAAT/enhancer binding protein-epsilon reduces atherosclerotic lesions in LDLR-/- Mice. PLoS ONE 9 (1) : -. ScholarBank@NUS Repository.
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. © 2014 Okamoto et al.
Source Title: PLoS ONE
ISSN: 19326203
DOI: 10.1371/journal.pone.0085341
Appears in Collections:Staff Publications

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