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J. Lipid Res.
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A more recent version of this article appeared on June 1, 2009 Originally published In Press as doi:10.1194/jlr.M800484-JLR200 on April 13, 2009

Papers In Press, published online ahead of print February 2, 2009
J. Lipid Res., doi:10.1194/jlr.M800484-JLR200
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Submitted on September 10, 2008
Revised on January 22, 2009
Accepted on February 2, 2009

TNF-alpha stimulates the ACAT1 expression in differentiating monocytes to promote the CE-laden cell formation

Lei Lei, Ying Xiong, Jia Chen, Jin-Bo Yang, Yi Wang, Xin-Ying Yang, Cantherine C. Y. Chang, Bao-Liang Song, Ta-Yuan Chang, and Bo-Liang Li

Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Institute of Biochemistry and Cell Biology, Shanghai, Shanghai 200031

Corresponding Author: blli{at}sibs.ac.cn

High levels of the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) are present in atherosclerotic lesions. TNF-alpha regulates expression of multiple genes involved in various stages of atherosclerosis, and exhibits proatherosclerotic and antiatherosclerotic properties. ACAT catalyzes the formation of cholesteryl esters in monocytes/macrophages, and promotes the foam cell formation at the early stage of atherosclerosis. We hypothesize that TNF-alpha may be involved in regulating the ACAT gene expression in monocytes/macrophages. In the current manuscript, we show that in cultured, differentiating human monocytes, TNF-alpha enhances the expression of ACAT1 but not ACAT2 gene, increases the cholesteryl ester accumulation and promotes the lipid-laden cell formation. Several other proinflammatory cytokines tested do not affect the ACAT1 gene expression. The stimulation effect is consistent with a receptor dependent process, and is blocked by using nuclear factor-kappa B (NF-kappa B) inhibitors. A functional and unique NF-kappa B element located within the human ACAT1 gene proximal promoter is required to mediate the action of TNF-alpha. Our data demonstrate that TNF-alpha, through the NF-kappa B pathway, specifically enhances the expression of human ACAT1 gene to promote the CE-laden cell formation from the differentiating monocytes, and support the hypothesis that TNF-alpha is proatherosclerotic during early phase of lesion development.


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