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 |
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| Authors: | H. Zhang J. Chen X. Liu L. Awar A. McMickle F. Bai S. Nagarajan S. Yu |
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| Affiliation: | 1. Arkansas Biosciences Institute, Department of Biological Science, Arkansas State University, , Jonesboro, AR, USA;2. Department of Bioscience and Bioengineering, Dalian University of Technology, , Dalian, China;3. Department of Veterinary Pathobiology, University of Missouri‐Columbia, , Columbia, MO, USA;4. Department of Pharmacology and Physiology, University of Missouri‐Columbia, , Columbia, MO, USA;5. Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, , Little Rock, AR, USA;6. Department of Pathology, University of Pittsburgh, , Pittsburgh, PA, USA |
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| 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‐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. |
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