Document Detail

Pro-inflammatory effects of interleukin-17A on vascular smooth muscle cells involve NAD(P)H- oxidase derived reactive oxygen species.
MedLine Citation:
PMID:  20606471     Owner:  NLM     Status:  MEDLINE    
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.
Eweline Pietrowski; Bianca Bender; Jula Huppert; Robin White; Heiko J Luhmann; Christoph R W Kuhlmann
Publication Detail:
Type:  Journal Article     Date:  2010-07-06
Journal Detail:
Title:  Journal of vascular research     Volume:  48     ISSN:  1423-0135     ISO Abbreviation:  J. Vasc. Res.     Publication Date:  2011  
Date Detail:
Created Date:  2010-12-14     Completed Date:  2011-01-19     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9206092     Medline TA:  J Vasc Res     Country:  Switzerland    
Other Details:
Languages:  eng     Pagination:  52-8     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 S. Karger AG, Basel.
Institute of Physiology and Pathophysiology, University Medical Center of the Johannes Gutenberg University, Mainz, Germany.
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MeSH Terms
Acetophenones / pharmacology
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, 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
Reg. No./Substance:
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 protein, mouse; EC Oxidase; EC Mitogen-Activated Protein Kinases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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