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http://dx.doi.org/10.5483/BMBRep.2012.45.7.088

Increased expression of interleukin-1β in triglyceride-induced macrophage cell death is mediated by p38 MAP kinase  

Sung, Ho-Joong (Department of Biomedical Laboratory Science, College of Health Science, Eulji University)
Son, Sin-Jee (Department of Biomedical Laboratory Science, College of Health Sciences, Yonsei University)
Yang, Seung-Ju (Department of Biomedical Laboratory Science, Konyang University)
Rhee, Ki-Jong (Department of Biomedical Laboratory Science, College of Health Sciences, Yonsei University)
Kim, Yoon-Suk (Department of Biomedical Laboratory Science, College of Health Sciences, Yonsei University)
Publication Information
BMB Reports / v.45, no.7, 2012 , pp. 414-418 More about this Journal
Abstract
Triglycerides (TG) are implicated in the development of atherosclerosis through formation of foam cells and induction of macrophage cell death. In this study, we report that addition of exogenous TG induced cell death in phorbol 12-myristate 13-acetate-differentiated THP-1 human macrophages. TG treatment induced a dramatic decrease in interleukin-$1{\beta}$ (IL-$1{\beta}$) mRNA expression in a dose- and time-dependent manner. The expression of granulocyte macrophage colony-stimulating factor and platelet endothelial cell adhesion molecule remained unchanged. To identify signaling pathways involved in TG-induced downregulation of IL-$1{\beta}$, we added p38 MAPK, protein kinase C (PKC) or c-Raf1 specific inhibitors. We found that inhibition of p38 MAPK alleviated the TG-induced downregulation of IL-$1{\beta}$, whereas inhibition of PKC and c-Raf1 had no effect. This is the first report showing decreased IL-$1{\beta}$ expression during TG-induced cell death in a human macrophage line. Our results suggest that downregulation of IL-$1{\beta}$ expression by TG-treated macrophages may play a role during atherogenesis.
Keywords
Cell death; IL-$1{\beta}$; Macrophage; p38 MAP kinase; Triglyceride;
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