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Wnt4 prevents apoptosis and inflammation of dental pulp cells induced by LPS by inhibiting the IKK/NF‑κB pathway

  • Authors:
    • Chengli Ni
    • Gang Wu
    • Tingting Miao
    • Jianguang Xu
  • View Affiliations / Copyright

    Affiliations: College of Stomatology, Anhui Medical College, Hefei, Anhui 230601, P.R. China, Shanghai Smartee Denti‑Technology Co., Ltd., Shanghai 200120, P.R. China, Key Laboratory of Oral Disease Research of Anhui Province, Department of Orthodontics, Stomatologic Hospital and College, Anhui Medical University, Hefei, Anhui 230032, P.R. China
    Copyright: © Ni et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 75
    |
    Published online on: December 23, 2022
       https://doi.org/10.3892/etm.2022.11774
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Abstract

Wnt4 has been shown to promote the recovery of odontogenic differentiation of dental pulp stem cells under inflammatory conditions, but its role in inflammation and apoptosis of pulpitis remains to be elucidated. Lipopolysaccharide (LPS) (10 µg/ml) was applied to treat the human dental pulp cells (HDPCs) for 24 h. Western blotting measured the expressions of inflammatory cytokines and apoptosis‑related proteins. Cell apoptosis was measured by flow cytometry. The level of Wnt4 was evaluated by reverse transcription‑quantitative PCR and western blotting. The results indicated that LPS could promote inflammatory response and apoptosis in HDPCs and downregulated Wnt4 expression was found in LPS‑HDPCs. Overexpression of Wnt4 ameliorated cell inflammatory response and apoptosis, presented by reduced expressions of IL‑8, IL‑6, TNF‑α, IL‑1β, Bax, cleaved‑caspase 3 and enhanced Bcl‑2 expression as well as decreased apoptosis rate. Moreover, overexpression of Wnt4 reduced the phosphorylation levels of IKK2, IκBα and p65 proteins upregulated by LPS. Finally, overexpression of IKK2 reversed the effects of Wnt4 on inflammation and apoptosis of LPS‑HDPCs and NF‑κB inhibitor reversed the effect of IKK2 overexpression in LPS‑HDPCs. Wnt4 inhibited LPS‑triggered inflammation and apoptosis in HDPCs via regulating the IKK/NF‑κB signaling pathway, which provided a new viewpoint for understanding the pathological mechanism of pulpitis.
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Copy and paste a formatted citation
Spandidos Publications style
Ni C, Wu G, Miao T and Xu J: Wnt4 prevents apoptosis and inflammation of dental pulp cells induced by LPS by inhibiting the IKK/NF‑κB pathway. Exp Ther Med 25: 75, 2023.
APA
Ni, C., Wu, G., Miao, T., & Xu, J. (2023). Wnt4 prevents apoptosis and inflammation of dental pulp cells induced by LPS by inhibiting the IKK/NF‑κB pathway. Experimental and Therapeutic Medicine, 25, 75. https://doi.org/10.3892/etm.2022.11774
MLA
Ni, C., Wu, G., Miao, T., Xu, J."Wnt4 prevents apoptosis and inflammation of dental pulp cells induced by LPS by inhibiting the IKK/NF‑κB pathway". Experimental and Therapeutic Medicine 25.2 (2023): 75.
Chicago
Ni, C., Wu, G., Miao, T., Xu, J."Wnt4 prevents apoptosis and inflammation of dental pulp cells induced by LPS by inhibiting the IKK/NF‑κB pathway". Experimental and Therapeutic Medicine 25, no. 2 (2023): 75. https://doi.org/10.3892/etm.2022.11774
Copy and paste a formatted citation
x
Spandidos Publications style
Ni C, Wu G, Miao T and Xu J: Wnt4 prevents apoptosis and inflammation of dental pulp cells induced by LPS by inhibiting the IKK/NF‑κB pathway. Exp Ther Med 25: 75, 2023.
APA
Ni, C., Wu, G., Miao, T., & Xu, J. (2023). Wnt4 prevents apoptosis and inflammation of dental pulp cells induced by LPS by inhibiting the IKK/NF‑κB pathway. Experimental and Therapeutic Medicine, 25, 75. https://doi.org/10.3892/etm.2022.11774
MLA
Ni, C., Wu, G., Miao, T., Xu, J."Wnt4 prevents apoptosis and inflammation of dental pulp cells induced by LPS by inhibiting the IKK/NF‑κB pathway". Experimental and Therapeutic Medicine 25.2 (2023): 75.
Chicago
Ni, C., Wu, G., Miao, T., Xu, J."Wnt4 prevents apoptosis and inflammation of dental pulp cells induced by LPS by inhibiting the IKK/NF‑κB pathway". Experimental and Therapeutic Medicine 25, no. 2 (2023): 75. https://doi.org/10.3892/etm.2022.11774
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