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IL ‐17 Induces Expression of Vascular Cell Adhesion Molecule Through Signalling Pathway of NF ‐κB, but not Akt1 and TAK 1 in Vascular Smooth Muscle Cells
Author(s) -
Zhang H.,
Chen J.,
Liu X.,
Awar L.,
McMickle A.,
Bai F.,
Nagarajan S.,
Yu S.
Publication year - 2013
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/sji.12030
Subject(s) - downregulation and upregulation , vascular smooth muscle , vcam 1 , microbiology and biotechnology , nf κb , cell adhesion molecule , akt1 , signal transduction , cell adhesion , gene silencing , transfection , inflammation , effector , biology , chemistry , cancer research , cell , immunology , smooth muscle , pi3k/akt/mtor pathway , cell culture , icam 1 , endocrinology , gene , biochemistry , genetics
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 ( SMC s), 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 SMC s is dependent on NF ‐κB, but independent of Akt1 and TAK 1. This is because knocking down A kt1 or TAK 1 by si RNA did not reduce IL ‐17‐induced activation of NF ‐κB and expression of VCAM ‐1, whereas knocking down NF ‐κB by si RNA 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 ERK 1/2. Therefore, these signalling pathways of IL ‐17‐mediated upregulation of VCAM ‐1 expression might be therapeutic targets for treatment of IL ‐17‐mediated inflammation.