N-3-oxododecanoyl homoserine lactone exacerbates endothelial cell death by inducing receptor-interacting protein kinase 1-dependent apoptosis
DC Field | Value | Language |
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dc.contributor.author | Shin, Jungho | - |
dc.contributor.author | Ahn, Sun Hee | - |
dc.contributor.author | Kim, Su Hyun | - |
dc.contributor.author | Oh, Dong-Jin | - |
dc.date.accessioned | 2022-07-06T12:03:22Z | - |
dc.date.available | 2022-07-06T12:03:22Z | - |
dc.date.created | 2021-12-08 | - |
dc.date.issued | 2021-10 | - |
dc.identifier.issn | 0363-6143 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/140805 | - |
dc.description.abstract | Endothelial dysfunction is associated with the initiation of sepsis-associated organ failure. Bacterial quorum-sensing molecules act as pathogen-associated molecular patterns; however, the effects of quorum-sensing molecules on endothelial cells remain less understood. This study investigated the molecular mechanisms of quorum-sensing molecule-induced cell death and their interaction with lipopolysaccharide (LPS) in human umbilical vein endothelial cells. Endothelial cells were treated with N-3-oxodo-decanoyl homoserine lactone (3OC12-HSL) and LPS derived from Pseudomonas aeruginosa. Treatment with 3OC12-HSL reduced cell viability in a dose-dependent manner, and cotreatment with 3OC12-HSL and LPS enhanced cell death. Terminal deoxynu-cleotidyl transferase deoxyuridine triphosphate nick end labeling assay revealed an increase in apoptotic cell death following 3OC12-HSL treatment; furthermore, cotreatment with 3OC12-HSL and LPS enhanced apoptosis. Western blotting revealed that treatment with 3OC12-HSL activated the receptor-interacting protein kinase 1 (RIPK1) pathway, leading to an increase in the levels of cleaved caspase 8 and 3. In addition, we found that treatment with necrostatin-1, an RIPK1 inhibitor, reduced cell death and ameliorated the activation of the RIPK1-dependent apoptotic pathway in 3OC12-HSL-treated cells. In conclusion, 3OC12-HSL induced endothelial cell apoptosis via the activation of the RIPK1 pathway, independent of LPS toxicity. Inhibition of RIPK1 may act as a therapeutic option for preserving endothelial cell integrity in patients with sepsis by disrupting the mechanism by which quorum-sensing molecules mediate their toxicity. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | AMER PHYSIOLOGICAL SOC | - |
dc.title | N-3-oxododecanoyl homoserine lactone exacerbates endothelial cell death by inducing receptor-interacting protein kinase 1-dependent apoptosis | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Oh, Dong-Jin | - |
dc.identifier.doi | 10.1152/ajpcell.00094.2021 | - |
dc.identifier.scopusid | 2-s2.0-85115765430 | - |
dc.identifier.wosid | 000704984000001 | - |
dc.identifier.bibliographicCitation | AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, v.321, no.4, pp.C644 - C653 | - |
dc.relation.isPartOf | AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY | - |
dc.citation.title | AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY | - |
dc.citation.volume | 321 | - |
dc.citation.number | 4 | - |
dc.citation.startPage | C644 | - |
dc.citation.endPage | C653 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalResearchArea | Physiology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Physiology | - |
dc.subject.keywordPlus | NF-KAPPA-B | - |
dc.subject.keywordPlus | SEPTIC SHOCK | - |
dc.subject.keywordPlus | PSEUDOMONAS | - |
dc.subject.keywordPlus | INFLAMMATION | - |
dc.subject.keywordPlus | DISRUPTION | - |
dc.subject.keywordPlus | MODULATION | - |
dc.subject.keywordPlus | MECHANISM | - |
dc.subject.keywordPlus | RESPONSES | - |
dc.subject.keywordPlus | ELASTASE | - |
dc.subject.keywordPlus | ROLES | - |
dc.subject.keywordAuthor | endothelial cell | - |
dc.subject.keywordAuthor | lipopolysaccharide | - |
dc.subject.keywordAuthor | N-3-oxododecanoyl homoserine lactone | - |
dc.subject.keywordAuthor | quorum-sensing molecule | - |
dc.subject.keywordAuthor | receptor-interacting pro-tein kinase 1 | - |
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