Document Detail


IL-17 induces expression of vascular cell adhesion molecule through signalling pathway of NF-κB, but not Akt1 and TAK1 in vascular smooth muscle cells.
MedLine Citation:
PMID:  23421430     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Interleukin-17 (IL-17) plays an important role in several autoimmune diseases. IL-17 can induce the expression of vascular cell adhesion molecule (VCAM-1) in aortic vascular smooth muscle cells (SMCs), which is important for the development of atherosclerosis. However, the signalling pathway of IL-17-induced VCAM-1 expression remains unclear. In this study, we reported that IL-17-induced expression of VCAM-1 in SMCs is dependent on NF-κB, but independent of Akt1 and TAK1. This is because knocking down Akt1 or TAK1 by siRNA did not reduce IL-17-induced activation of NF-κB and expression of VCAM-1, whereas knocking down NF-κB by siRNA markedly inhibited IL-17-mediated upregulation of VCAM-1 expression. In addition, IL-17-induced expression of VCAM-1 is partially dependent on activation of ERK1/2. Therefore, these signalling pathways of IL-17-mediated upregulation of VCAM-1 expression might be therapeutic targets for treatment of IL-17-mediated inflammation.
Authors:
H Zhang; J Chen; X Liu; L Awar; A McMickle; F Bai; S Nagarajan; S Yu
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.    
Journal Detail:
Title:  Scandinavian journal of immunology     Volume:  77     ISSN:  1365-3083     ISO Abbreviation:  Scand. J. Immunol.     Publication Date:  2013 Apr 
Date Detail:
Created Date:  2013-03-26     Completed Date:  2013-05-15     Revised Date:  2014-04-02    
Medline Journal Info:
Nlm Unique ID:  0323767     Medline TA:  Scand J Immunol     Country:  England    
Other Details:
Languages:  eng     Pagination:  230-7     Citation Subset:  IM    
Copyright Information:
© 2013 The Authors. Scandinavian Journal of Immunology © 2013 Blackwell Publishing Ltd.
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MeSH Terms
Descriptor/Qualifier:
Animals
Gene Expression Regulation / drug effects
Gene Silencing
Humans
Intercellular Adhesion Molecule-1 / genetics
Interleukin-17 / pharmacology*
MAP Kinase Kinase Kinases / metabolism
MAP Kinase Signaling System
Muscle, Smooth, Vascular / metabolism*
Myocytes, Smooth Muscle / drug effects*,  metabolism*
NF-kappa B / genetics,  metabolism*
Proto-Oncogene Proteins c-akt / metabolism
RNA, Small Interfering / genetics,  metabolism
Rats
Signal Transduction / drug effects*
TNF Receptor-Associated Factor 3 / genetics,  metabolism
Transcription Factor RelA / genetics,  metabolism
Vascular Cell Adhesion Molecule-1 / genetics*
Grant Support
ID/Acronym/Agency:
P20 GM103429/GM/NIGMS NIH HHS; P20GM103429/GM/NIGMS NIH HHS; R01 HL086674/HL/NHLBI NIH HHS; R01-HL086674/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Interleukin-17; 0/NF-kappa B; 0/RNA, Small Interfering; 0/TNF Receptor-Associated Factor 3; 0/Transcription Factor RelA; 0/Vascular Cell Adhesion Molecule-1; 126547-89-5/Intercellular Adhesion Molecule-1; EC 2.7.11.1/AKT1 protein, human; EC 2.7.11.1/Proto-Oncogene Proteins c-akt; EC 2.7.11.25/MAP Kinase Kinase Kinases; EC 2.7.11.25/MAP kinase kinase kinase 7
Comments/Corrections

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