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. 2010 Apr 23;31(18):2301–2309. doi: 10.1093/eurheartj/ehq107

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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2010. For permissions please email: journals.permissions@oxfordjournals.org

The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that the original authorship is properly and fully attributed; the Journal, Learned Society and Oxford University Press are attributed as the original place of publication with correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org

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Deacetylation of RelA/p65 by SIRT1 diminishes Lox-1 expression. (A) Aortic Lox-1 expression is increased in ApoE^−/− SIRT1^+/− compared with ApoE^−/− SIRT1^+/+ mice. (B) Lox-1 expression is higher in 5 h TNFα-stimulated RAW 264.7 macrophages pretreated with 200 µM splitomicin (Splito) compared with untreated cells (nt). (C) Ectopic SIRT1 expression in SIRT1^−/− MEF reduces Lox-1 expression. (D) In RelA/p65^−/− MEF with reconstituted wt-RelA/p65, siRNA-mediated SIRT1 knockdown enhances Lox-1 expression upon 5 h TNFα stimulation, whereas no effect is observed in RelA/p65^−/− MEF with a reconstituted mutated, non-acetylatable K310-RelA/p65. *P < 0.05; ***P < 0.001.