Very low density lipoprotein potentiates tumor necrosis factor-α expression in macrophages

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Very low density lipoprotein potentiates tumor necrosis factor-α expression in macrophages

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Publication Article, peer reviewed scientific
Title Very low density lipoprotein potentiates tumor necrosis factor-α expression in macrophages
Author(s) Stollenwerk, Maria M ; Schiopu, A ; Nordin Fredrikson, Gunilla ; Dichtl, W ; Nilsson, J ; Ares, Mikko PS
Date 2005
English abstract
High levels of the triacylglycerol-rich lipoproteins, very low density lipoprotein (VLDL) and intermediate density lipoprotein (IDL) have been identified as independent risk factors for coronary heart disease, and inflammation is thought to contribute to atherosclerosis and its complications. To understand how dyslipidemia promotes inflammation, we have characterised the effects of VLDL treatment on production of tumor necrosis factor-α (TNF) by human monocyte-derived macrophages. VLDL strongly potentiated lipopolysaccharide (LPS)-induced expression of TNF mRNA and secretion of TNF protein. VLDL activated mitogen-activated protein kinase-ERK kinase 1/2 (MEK1/2), and potentiated LPS-induced MEK1/2 activation. The MEK1/2 inhibitor U0126 strongly diminished TNF expression, indicating that MEK1/2 plays a central role in the regulation of TNF expression. VLDL did not activate transcription factors NF-κB and PPAR-γ, but it activated AP-1 at least as potently as LPS, and potentiated LPS-induced activation of AP-1. The inhibitor U0126 completely prevented this potentiation. Inhibition of AP-1 by decoy oligonucleotides abolished potentiation of TNF secretion by VLDL. In conclusion, VLDL treatment potentiates TNF expression in macrophages by activation of MEK1/2 and AP-1. These findings suggest that triacylglycerol-rich lipoproteins are involved in inflammatory processes associated with atherosclerosis.
DOI http://dx.doi.org/10.1016/j.atherosclerosis.2004.12.002 (link to publisher's fulltext)
Publisher Elsevier Ireland Ltd.
Host/Issue Atheroschlerosis;2
Volume 179
ISSN 0021-9150
Pages 247-254
Language eng (iso)
Subject(s) Medicine
Handle http://hdl.handle.net/2043/2681 (link to this page)

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