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Wnt-C59 inhibits proinflammatory cytokine expression by reducing the interaction between β-catenin and NF-κB in LPS-stimulated epithelial and macrophage cellsopen accessWnt-C59 inhibits proinflammatory cytokine expression by reducing the interaction between β-catenin and NF-κB in LPS-stimulated epithelial and macrophage cells

Authors
Jang, JaewoongSong, JaewonSim, InaeYoon, Yoosik
Issue Date
Jul-2021
Publisher
대한약리학회
Keywords
Catenins; Cytokines; Inflammation; NF-kappa B
Citation
The Korean Journal of Physiology & Pharmacology, v.25, no.4, pp 307 - 319
Pages
13
Journal Title
The Korean Journal of Physiology & Pharmacology
Volume
25
Number
4
Start Page
307
End Page
319
URI
https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/50490
DOI
10.4196/kjpp.2021.25.4.307
ISSN
1226-4512
2093-3827
Abstract
Dysregulation of the Wnt pathway causes various diseases including cancer, Parkinson’s disease, Alzheimer’s disease, schizophrenia, osteoporosis, obesity and chronic kidney diseases. The modulation of dysregulated Wnt pathway is absolutely necessary. In the present study, we evaluated the anti-inflammatory effect and the mechanism of action of Wnt-C59, a Wnt signaling inhibitor, in lipopolysaccharide (LPS)-stimulated epithelial cells and macrophage cells. Wnt-C59 showed a dose-dependent anti-inflammatory effect by suppressing the expression of proinflammatory cytokines including IL6, CCL2, IL1A, IL1B, and TNF in LPS-stimulated cells. The dysregulation of the Wnt/-catenin pathway in LPS stimulated cells was suppressed by Wnt- C59 treatment. The level of -catenin, the executor protein of Wnt/-catenin pathway, was elevated by LPS and suppressed by Wnt-C59. Overexpression of -catenin rescued the suppressive effect of Wnt-C59 on proinflammatory cytokine expression and nuclear factor-kappa B (NF-B) activity. We found that the interaction between -catenin and NF-B, measured by co-immunoprecipitation assay, was elevated by LPS and suppressed by Wnt-C59 treatment. Both NF-B activity for its target DNA binding and the reporter activity of NF-B-responsive promoter showed identical patterns with the interaction between -catenin and NF-B. Altogether, our findings suggest that the anti-inflammatory effect of Wnt-C59 is mediated by the reduction of the cellular level of -catenin and the interaction between -catenin and NF-B, which results in the suppressions of the NF-B activity and proinflammatory cytokine expression.
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