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Papers In Press, published online ahead of print November 16, 2004
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Research Institute for Internal Medicine, University of Oslo, Oslo, Oslo 0027
Corresponding Author: bente.halvorsen{at}klinmed.uio.no
Abstract Interleukin (IL)-10 may have a therapeutic potential in atherosclerosis, but its mechanisms of action are not clarified. Foam cell formation is a key event in atherogenesis, and apoptosis of these lipid-laden cells may also promote plaque destabilization. We sought to explore whether IL-10 could have plaque-stabilizing properties in acute coronary syndromes (ACS). We studied the effect of IL-10 on oxidized (ox) LDL-stimulated THP-1 cells and monocyte-derived macrophages from ACS patients and healthy controls by different experimental approaches. Our main findings were: (i) IL-10 enhances lipid accumulation in oxLDL-stimulated THP-1 macrophages at least partly by counteracting oxLDL-induced apoptosis. (ii) This anti-apoptotic effect of IL-10 involves increased expression of the anti-apoptotic genes Bfl-1 and Mcl-1 accompanied by protective effects on mitochondria function. (iii) By silencing Bfl-1 and Mcl-1 gene using siRNAs we were able to abolish this IL-10-mediated effect on lipid accumulation. (iv) IL-10 also induced lipid accumulation in oxLDL-stimulated macrophages from patients with ACS, but not in macrophages from healthy controls. (v) In ACS patients this enhancing effect of IL-10 on lipid accumulation was accompanied by enhanced Mcl-1 expression. No such anti-apoptotic effect was seen in macrophages from healthy controls. Conclusion: These findings suggest a new mechanism for the effect of IL-10 in atherosclerosis, possibly contributing to plaque stabilization.
Revised on October 15, 2004
Accepted on November 2, 2004
Interleukin-10 enhances the oxidized LDL-induced foam cell formation of macrophages by anti-apoptotic mechanisms
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