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IL-17 induces expression of vascular cell adhesion molecule through signalling pathway of NF-?B, but not Akt1 and TAK1 in vascular smooth muscle cells.

ABSTRACT: 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-?B, 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-?B and expression of VCAM-1, whereas knocking down NF-?B 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.

SUBMITTER: Zhang H

PROVIDER: S-EPMC3683581 | biostudies-literature | 2013 Apr

REPOSITORIES: biostudies-literature

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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.

Zhang H H Chen J J Liu X X Awar L L McMickle A A Bai F F Nagarajan S S Yu S S

Scandinavian journal of immunology 20130401 4

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 knockin ...[more]

PMID: 23421430

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Project description:Asthma exacerbations are commonly associated with rhinovirus (RV) infection. Interleukin-33 (IL-33) plays an important role during exacerbation by enhancing Type 2 inflammation. Recently we showed that RV infects bronchial smooth muscle cells (BSMCs) triggering production of interferons and IL-33. Here we compared levels of RV-induced IL-33 in BSMCs from healthy and asthmatic subjects, and explored the involvement of pattern-recognition receptors (PRRs) and downstream signalling pathways in IL-33 expression. BSMCs from healthy and severe and non-severe asthmatic patients were infected with RV1B or stimulated with the PRR agonists poly(I:C) (Toll-like receptor 3 (TLR3)), imiquimod (TLR7) and poly(I:C)/LyoVec (retinoic acid-inducible gene 1 (RIG-I)/melanoma differentiation-associated protein 5 (MDA5)). Knockdown of TLR3, RIG-I and MDA5 was performed, and inhibitors targeting TBK1, nuclear factor-κB (NF-κB) and transforming growth factor (TGF)-β-activated kinase 1 (TAK1) were used. Gene and protein expression were assessed. RV triggered IL-33 gene and protein expression in BSMCs. BSMCs from patients with non-severe asthma showed higher baseline and RV-induced IL-33 gene expression compared to cells from patients with severe asthma and healthy controls. Furthermore, RV-induced IL-33 expression in BSMCs from healthy and asthmatic individuals was attenuated by knockdown of TLR3. Inhibition of TAK1, but not NF-κB or TBK1, limited RV-induced IL-33. The cytokine secretion profile showed higher production of IL-33 in BSMCs from patients with non-severe asthma compared to healthy controls upon RV infection. In addition, BSMCs from patients with non-severe asthma had higher levels of RV-induced IL-8, TNF-α, IL-1β, IL-17A, IL-5 and IL-13. RV infection caused higher levels of IL-33 and increased pro-inflammatory and Type 2 cytokine release in BSMCs from patients with non-severe asthma. RV-induced IL-33 expression was mainly regulated by TLR3 and downstream via TAK1. These signalling molecules represent potential therapeutic targets for treating asthma exacerbations.

Dataset Information

IL-17 induces expression of vascular cell adhesion molecule through signalling pathway of NF-?B, but not Akt1 and TAK1 in vascular smooth muscle cells.

Publications

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.

Similar Datasets

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