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Interleukin‑Iβ promotes cartilage degeneration by regulating forkhead box protein O4 and type Ⅱ collagen

  • Authors:
    • Jianxiong Wu
    • Hongjun Zhang
    • Rulin Deng
    • Lifeng Xing
    • Mingwu Hu
    • Xiaoling Fu
  • View Affiliations / Copyright

    Affiliations: Department of Emergency Medicine, Sir Run Run Shaw Hospital, Affiliated with The Zhejiang University School of Medicine, Hangzhou, Zhejiang 310085, P.R. China, Department of Orthopedics, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330008, P.R. China, Department of Orthopedics, Nanchang Hongdu Hospital of Traditional Chinese Medicine, Nanchang, Jiangxi 330038, P.R. China
    Copyright: © Wu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 813
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    Published online on: September 20, 2021
       https://doi.org/10.3892/mmr.2021.12453
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Abstract

Osteoarthritis (OA) is one of the most prevalent pain‑inducing and disabling diseases globally. Aging is a primary contributing factor to the progression of OA. Forkhead box protein O4 (FOXO4) is known to be involved in the cell cycle and apoptosis regulation. The aim of the present study was to investigate the association between FOXO4 expression and chondrocyte degeneration in rats. Chondrocytes were assigned to the control (4‑week‑old rats), natural degeneration (16‑week‑old rats) or induced degeneration (IL‑1β‑treated chondrocytes from 4‑week‑old rats) groups. Immunocytochemical analysis with β‑galactosidase staining revealed a greater number of stained cells present in the natural and induced degeneration groups than in the control group. PCR analysis indicated lower mRNA expression levels of collagen type II α1 chain (Col2α) and higher levels of FOXO4, and western blotting revealed reduced Col2α protein expression levels and significantly elevated FOXO4 levels in the natural and induced degeneration groups, compared with those in the control group. The results of the present study revealed that FOXO4 expression was altered in the natural and induced degeneration groups, and further research and exploration are needed to clarify the underlying mechanism.
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Copy and paste a formatted citation
Spandidos Publications style
Wu J, Zhang H, Deng R, Xing L, Hu M and Fu X: Interleukin‑Iβ promotes cartilage degeneration by regulating forkhead box protein O4 and type Ⅱ collagen. Mol Med Rep 24: 813, 2021.
APA
Wu, J., Zhang, H., Deng, R., Xing, L., Hu, M., & Fu, X. (2021). Interleukin‑Iβ promotes cartilage degeneration by regulating forkhead box protein O4 and type Ⅱ collagen. Molecular Medicine Reports, 24, 813. https://doi.org/10.3892/mmr.2021.12453
MLA
Wu, J., Zhang, H., Deng, R., Xing, L., Hu, M., Fu, X."Interleukin‑Iβ promotes cartilage degeneration by regulating forkhead box protein O4 and type Ⅱ collagen". Molecular Medicine Reports 24.5 (2021): 813.
Chicago
Wu, J., Zhang, H., Deng, R., Xing, L., Hu, M., Fu, X."Interleukin‑Iβ promotes cartilage degeneration by regulating forkhead box protein O4 and type Ⅱ collagen". Molecular Medicine Reports 24, no. 5 (2021): 813. https://doi.org/10.3892/mmr.2021.12453
Copy and paste a formatted citation
x
Spandidos Publications style
Wu J, Zhang H, Deng R, Xing L, Hu M and Fu X: Interleukin‑Iβ promotes cartilage degeneration by regulating forkhead box protein O4 and type Ⅱ collagen. Mol Med Rep 24: 813, 2021.
APA
Wu, J., Zhang, H., Deng, R., Xing, L., Hu, M., & Fu, X. (2021). Interleukin‑Iβ promotes cartilage degeneration by regulating forkhead box protein O4 and type Ⅱ collagen. Molecular Medicine Reports, 24, 813. https://doi.org/10.3892/mmr.2021.12453
MLA
Wu, J., Zhang, H., Deng, R., Xing, L., Hu, M., Fu, X."Interleukin‑Iβ promotes cartilage degeneration by regulating forkhead box protein O4 and type Ⅱ collagen". Molecular Medicine Reports 24.5 (2021): 813.
Chicago
Wu, J., Zhang, H., Deng, R., Xing, L., Hu, M., Fu, X."Interleukin‑Iβ promotes cartilage degeneration by regulating forkhead box protein O4 and type Ⅱ collagen". Molecular Medicine Reports 24, no. 5 (2021): 813. https://doi.org/10.3892/mmr.2021.12453
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