High mobility group box-1 promotes inflammation in endometriotic stromal cells through Toll-like receptor 4/nuclear factor-kappa B
DC Field | Value | Language |
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dc.contributor.author | Yun, Bo Hyon | - |
dc.contributor.author | Kim, Sunghoon | - |
dc.contributor.author | Chon, Seung Joo | - |
dc.contributor.author | Kim, Ga Hee | - |
dc.contributor.author | Choi, Young Sik | - |
dc.contributor.author | Cho, SiHyun | - |
dc.contributor.author | Lee, Byung Seok | - |
dc.contributor.author | Seo, Seok Kyo | - |
dc.date.available | 2021-04-14T00:40:19Z | - |
dc.date.created | 2021-03-29 | - |
dc.date.issued | 2021-03 | - |
dc.identifier.issn | 1943-8141 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/80725 | - |
dc.description.abstract | Objective: To investigate whether high-mobility group box-1 induces cell proliferation, invasion and mediates inflammation in ectopic human endometrial stromal cells through Toll-like receptor 4. Methods: Ectopic endometrial specimens were retrieved from patients with ovarian endometrioma having laparoscopy. Ectopic HESCs were treated with H2O2and recombinant HMGB-1 to induce oxidative stress. The effect of oxidative stress on cell proliferation and invasion was demonstrated. Receptors for HMGB-1 in NF-κB pathway (TLR4, RAGE), angiogenic molecule (VEGF), adhesion molecules (ICAM-1, E-cadherin), and inflammatory cytokines were measured simultaneously to the oxidative stress. Results: Ectopic HESCs showed markedly decreased cell viability with the increased release of HMGB-1 following treatment with H2O2. When ectopic HESCs were stressed by rHMGB-1, cell proliferation and cell migration numbers increased significantly in a dose-dependent manner. Increased TLR4 and RAGE mRNA and protein expression levels were noted to rHMGB-1 treatment in a dose-dependent manner. VEGF synthesis was also increased by rHMGB-1 treatment. The gene expression of ICAM-1 was upregulated, whereas that of E-cadherin was downregulated with rHMGB-1 treatment. Interleukin-6, IL-1β, tumor necrosis factor-alpha, and IL-10 were increased significantly by rHMGB-1 treatment. Inversely, after transfection of small interfering RNA against TLR4, rHMGB treatment resulted in decreased cell proliferation and invasion. Conclusion: HMGB-1 activates the NF-κB pathway via TLR4 to increase cell proliferation, invasion, and the production of various inflammatory markers in HESCs. Thus, HMGB-1, TLR4, and NF-κB may represent potential therapeutic targets for the treatment of endometriosis. © 2021 E-Century Publishing Corporation. All rights reserved. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | E-Century Publishing Corporation | - |
dc.relation.isPartOf | American Journal of Translational Research | - |
dc.title | High mobility group box-1 promotes inflammation in endometriotic stromal cells through Toll-like receptor 4/nuclear factor-kappa B | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000631821600007 | - |
dc.identifier.bibliographicCitation | American Journal of Translational Research, v.13, no.3, pp.1400 - 1410 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.scopusid | 2-s2.0-85102873640 | - |
dc.citation.endPage | 1410 | - |
dc.citation.startPage | 1400 | - |
dc.citation.title | American Journal of Translational Research | - |
dc.citation.volume | 13 | - |
dc.citation.number | 3 | - |
dc.contributor.affiliatedAuthor | Chon, Seung Joo | - |
dc.identifier.url | http://www.ajtr.org/V13_No3.html | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | Endometriosis | - |
dc.subject.keywordAuthor | HMGB-1 | - |
dc.subject.keywordAuthor | Oxidative stress | - |
dc.subject.keywordAuthor | TLR4 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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