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High mobility group box-1 promotes inflammation in endometriotic stromal cells through Toll-like receptor 4/nuclear factor-kappa B

Authors
 Bo Hyon Yun  ;  Sunghoon Kim  ;  Seung Joo Chon  ;  Ga Hee Kim  ;  Young Sik Choi  ;  SiHyun Cho  ;  Byung Seok Lee  ;  Seok Kyo Seo 
Citation
 AMERICAN JOURNAL OF TRANSLATIONAL RESEARCH, Vol.13(3) : 1400-1410, 2021-03 
Journal Title
 AMERICAN JOURNAL OF TRANSLATIONAL RESEARCH 
Issue Date
2021-03
Keywords
Endometriosis ; HMGB-1 ; TLR4 ; oxidative stress
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 H2O2 and 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.
Files in This Item:
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Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Obstetrics and Gynecology (산부인과학교실) > 1. Journal Papers
Yonsei Authors
Kim, Sung Hoon(김성훈) ORCID logo https://orcid.org/0000-0002-1645-7473
Seo, Seok Kyo(서석교) ORCID logo https://orcid.org/0000-0003-3404-0484
Yun, Bo Hyon(윤보현) ORCID logo https://orcid.org/0000-0001-5703-797X
Lee, Byung Seok(이병석) ORCID logo https://orcid.org/0000-0001-6001-2079
Cho, Si Hyun(조시현) ORCID logo https://orcid.org/0000-0003-2718-6645
Choi, Young Sik(최영식) ORCID logo https://orcid.org/0000-0002-1157-4822
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/182457
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