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Sökning: id:"swepub:oai:DiVA.org:mau-4186" > Very low density li...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00002974naa a2200337 4500
001oai:DiVA.org:mau-4186
003SwePub
008200228s2005 | |||||||||||000 ||eng|
024a https://urn.kb.se/resolve?urn=urn:nbn:se:mau:diva-41862 URI
024a https://doi.org/10.1016/j.atherosclerosis.2004.12.0022 DOI
040 a (SwePub)mau
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Stollenwerk, Maria M4 aut
2451 0a Very low density lipoprotein potentiates tumor necrosis factor-α expression in macrophages
264 1b Elsevier Ireland Ltd.c 2005
338 a print2 rdacarrier
520 a 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.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinsk bioteknologix Biomedicinsk laboratorievetenskap/teknologi0 (SwePub)304022 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Medical Biotechnologyx Biomedical Laboratory Science/Technology0 (SwePub)304022 hsv//eng
700a Schiopu, A4 aut
700a Nordin Fredrikson, Gunillau Malmö högskola,Fakulteten för hälsa och samhälle (HS)4 aut0 (Swepub:mau)hsguno
700a Dichtl, W4 aut
700a Nilsson, J4 aut
700a Ares, Mikko PS4 aut
710a Malmö högskolab Fakulteten för hälsa och samhälle (HS)4 org
773t Atherosclerosisd : Elsevier Ireland Ltd.g 179:2, s. 247-254q 179:2<247-254x 0021-9150x 1879-1484
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:mau:diva-4186
8564 8u https://doi.org/10.1016/j.atherosclerosis.2004.12.002

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