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- Title
Nur77 Decreases Atherosclerosis Progression in apoE<sup>−/−</sup> Mice Fed a High-Fat/High-Cholesterol Diet.
- Authors
Hu, Yan-Wei; Zhang, Peng; Yang, Jun-Yao; Huang, Jin-Lan; Ma, Xin; Li, Shu-Fen; Zhao, Jia-Yi; Hu, Ya-Rong; Wang, Yan-Chao; Gao, Ji-Juan; Sha, Yan-Hua; Zheng, Lei; Wang, Qian
- Abstract
Rationale: It is clear that lipid disorder and inflammation are associated with cardiovascular diseases and underlying atherosclerosis. Nur77 has been shown to be involved in inflammatory response and lipid metabolism. Objective: Here, we explored the role of Nur77 in atherosclerotic plaque progression in apoE−/− mice fed a high-fat/high cholesterol diet. Methods and Results: The Nur77 gene, a nuclear hormone receptor, was highly induced by treatment with Cytosporone B (Csn-B, specific Nur77 agonist), recombinant plasmid over-expressing Nur77 (pcDNA-Nur77), while inhibited by treatment with siRNAs against Nur77 (si-Nur77) in THP-1 macrophage-derived foam cells, HepG2 cells and Caco-2 cells, respectively. In addition, the expression of Nur77 was highly induced by Nur77 agonist Csn-B, lentivirus encoding Nur77 (LV-Nur77), while silenced by lentivirus encoding siRNA against Nur77 (si-Nur77) in apoE−/− mice fed a high-fat/high cholesterol diet, respectively. We found that increased expression of Nur77 reduced macrophage-derived foam cells formation and hepatic lipid deposition, downregulated gene levels of inflammatory molecules, adhesion molecules and intestinal lipid absorption, and decreases atherosclerotic plaque formation. Conclusion: These observations provide direct evidence that Nur77 is an important nuclear hormone receptor in regulation of atherosclerotic plaque formation and thus represents a promising target for the treatment of atherosclerosis.
- Publication
PLoS ONE, 2014, Vol 9, Issue 1, p1
- ISSN
1932-6203
- Publication type
Academic Journal
- DOI
10.1371/journal.pone.0087313