TLR4-mediated IRAK1 activation induces TNF-alpha expression via JNK-dependent NF-kappa B activation in human bronchial epithelial cells
DC Field | Value | Language |
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dc.contributor.author | Park, Sae Hoon | - |
dc.contributor.author | Choi, Hye-Jin | - |
dc.contributor.author | Lee, So Young | - |
dc.contributor.author | Han, Joong-Soo | - |
dc.date.accessioned | 2021-08-11T19:24:59Z | - |
dc.date.available | 2021-08-11T19:24:59Z | - |
dc.date.issued | 2015-12 | - |
dc.identifier.issn | 1721-727X | - |
dc.identifier.issn | 2058-7392 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/10090 | - |
dc.description.abstract | The purpose of this study was to identify the mechanism of lipopolysaccharide (LPS)-induced expression of tumor necrosis factor (TNF)-alpha in BEAS-2B. Toll-like receptor (TLR)4-specific siRNA was found to completely abolish the LPS-induced expression of MyD88 and TNF-alpha. There was enhanced binding of MyD88 with IRAK1 following LPS treatment, and MyD88- or IRAK1-specific siRNAs decreased the expression of TNF-alpha. In addition, IRAK1 siRNA downregulated the phosphorylation of PKC alpha, demonstrating that PKC alpha is a downstream effector of IRAK1. Inhibition of PKC alpha completely blocked the activation of AKT, whereas inhibition of AKT with a PI3K inhibitor prevented the LPS-induced expression of TNF-alpha. We found that AKT activated JNK, which then stimulated phosphorylation of I kappa-B alpha, resulting in NF-kappa B activation. As expected, inhibition of NF-kappa B completely inhibited the expression of TNF-alpha. Taken together, our results suggest that LPS induces TNF-alpha expression by activating NF-kappa B via the PKC/PI3K/AKT/JNK pathway, which is in turn dependent on MyD88/IRAK1. | - |
dc.format.extent | 13 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | Biolife | - |
dc.title | TLR4-mediated IRAK1 activation induces TNF-alpha expression via JNK-dependent NF-kappa B activation in human bronchial epithelial cells | - |
dc.type | Article | - |
dc.publisher.location | 미국 | - |
dc.identifier.doi | 10.1177/1721727X15619185 | - |
dc.identifier.wosid | 000365744100006 | - |
dc.identifier.bibliographicCitation | European Journal of Inflammation, v.13, no.3, pp 183 - 195 | - |
dc.citation.title | European Journal of Inflammation | - |
dc.citation.volume | 13 | - |
dc.citation.number | 3 | - |
dc.citation.startPage | 183 | - |
dc.citation.endPage | 195 | - |
dc.type.docType | Article | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Immunology | - |
dc.relation.journalWebOfScienceCategory | Immunology | - |
dc.subject.keywordPlus | TOLL-LIKE RECEPTOR | - |
dc.subject.keywordPlus | DERMAL ENDOTHELIAL-CELLS | - |
dc.subject.keywordPlus | SIGNALING PATHWAYS | - |
dc.subject.keywordPlus | PHOSPHATIDYLINOSITOL 3-KINASE | - |
dc.subject.keywordPlus | INFLAMMATORY RESPONSE | - |
dc.subject.keywordPlus | PHOSPHORYLATION | - |
dc.subject.keywordPlus | TRANSDUCTION | - |
dc.subject.keywordPlus | INHIBITION | - |
dc.subject.keywordPlus | MEDIATORS | - |
dc.subject.keywordPlus | OXIDASE | - |
dc.subject.keywordAuthor | IRAK1 | - |
dc.subject.keywordAuthor | JNK | - |
dc.subject.keywordAuthor | NF-kappa B | - |
dc.subject.keywordAuthor | TLR4 | - |
dc.subject.keywordAuthor | TNF-alpha | - |
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