| Pro-inflammatory effects of interleukin-17A on vascular smooth muscle cells involve NAD(P)H- oxidase derived reactive oxygen species. | |
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MedLine Citation:
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PMID: 20606471 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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T cells are known for their contribution to the inflammatory element of atherosclerosis. Recently, it has been demonstrated that the Th17 derived cytokine IL-17 is involved in the pro-inflammatory response of vascular smooth muscle cells (VSMC). The aim of the present study was to examine whether reactive oxygen species (ROS) might be involved in this context. The effect of IL-17A on ROS generation was examined using the fluorescent dye 2'7'-dichlorodihydrofluorescein (H(2)DCF) in primary murine VSMC. IL-17A induced an increase in H(2)DCF fluorescence in VSMC, and this effect was blocked by the NAD(P)H-oxidase inhibitor apocynin and siRNA targeting Nox2. The p38-MAPK inhibitors SB203580 and SB202190 dose-dependently reduced the IL-17A induced ROS production. The IL-17A induced release of the pro-inflammatory cytokines IL-6, G-CSF, GM-CSF and MCP-1 from VSMC, as detected by the Luminex technology, was completely abolished by NAD(P)H-oxidase inhibition. Taken together, our data indicate that IL-17A causes the NAD(P)H-oxidase dependent generation of ROS leading to a pro-inflammatory activation of VSMC. |
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Authors:
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Eweline Pietrowski; Bianca Bender; Jula Huppert; Robin White; Heiko J Luhmann; Christoph R W Kuhlmann |
Publication Detail:
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Type: Journal Article Date: 2010-07-06 |
Journal Detail:
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Title: Journal of vascular research Volume: 48 ISSN: 1423-0135 ISO Abbreviation: J. Vasc. Res. Publication Date: 2011 |
Date Detail:
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Created Date: 2010-12-14 Completed Date: 2011-01-19 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9206092 Medline TA: J Vasc Res Country: Switzerland |
Other Details:
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Languages: eng Pagination: 52-8 Citation Subset: IM |
Copyright Information:
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Copyright © 2010 S. Karger AG, Basel. |
Affiliation:
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Institute of Physiology and Pathophysiology, University Medical Center of the Johannes Gutenberg University, Mainz, Germany. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acetophenones
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pharmacology Animals Aorta, Thoracic / cytology Cell Differentiation / drug effects, physiology Cell Movement / drug effects, physiology Cells, Cultured Cytokines / metabolism Enzyme Inhibitors / pharmacology Interleukin-17 / metabolism*, pharmacology Membrane Glycoproteins / antagonists & inhibitors, genetics, metabolism* Mice Mice, Inbred C57BL Muscle, Smooth, Vascular / cytology, enzymology*, immunology* NADPH Oxidase / antagonists & inhibitors, genetics, metabolism* Oxidative Stress / drug effects, physiology RNA, Small Interfering Reactive Oxygen Species / metabolism* p38 Mitogen-Activated Protein Kinases / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Acetophenones; 0/Cytokines; 0/Enzyme Inhibitors; 0/Interleukin-17; 0/Membrane Glycoproteins; 0/RNA, Small Interfering; 0/Reactive Oxygen Species; 498-02-2/acetovanillone; EC 1.6.-/Nox4 protein, mouse; EC 1.6.3.1/Cybb protein, mouse; EC 1.6.3.1/NADPH Oxidase; EC 2.7.11.24/p38 Mitogen-Activated Protein Kinases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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