High mobility group box-1 promotes inflammation in endometriotic stromal cells through Toll-like receptor 4/nuclear factor-kappa B
- Authors
- Yun, Bo Hyon; Kim, Sunghoon; Chon, Seung Joo; Kim, Ga Hee; Choi, Young Sik; Cho, SiHyun; Lee, Byung Seok; Seo, Seok Kyo
- Issue Date
- Mar-2021
- Publisher
- E-Century Publishing Corporation
- Keywords
- Endometriosis; HMGB-1; Oxidative stress; TLR4
- Citation
- American Journal of Translational Research, v.13, no.3, pp.1400 - 1410
- Journal Title
- American Journal of Translational Research
- Volume
- 13
- Number
- 3
- Start Page
- 1400
- End Page
- 1410
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/80725
- ISSN
- 1943-8141
- 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.
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