4.5 Article

Based on G-Series Mouse TH17 Array Study the Effect of Fluoride on C2C12 Cells Cytokines Expression

期刊

BIOLOGICAL TRACE ELEMENT RESEARCH
卷 199, 期 9, 页码 3402-3410

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SPRINGERNATURE
DOI: 10.1007/s12011-020-02464-6

关键词

Fluoride; Th17-related cytokines; Antibody array; Immunity

资金

  1. National Natural Science Foundation of China [31201963]
  2. Natural Science Foundation of Henan [202300410120]

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The results of the experiment revealed that treatment with 2.5 mmol/L fluoride caused an upregulation of certain cytokines in skeletal muscle cells, including MIP-3 alpha, IL-21, and IL-13. This could induce cytotoxicity by disrupting the expression of Th17-related cytokines.
C2C12 cells were cultured on medium containing fluoride (0, 1, and 2.5 mmol/L) for 48 h to investigate the effect of excessive fluoride on T helper 17 (Th17)-related cytokine expression profile in skeletal muscle cells, and the culture supernatant was collected and subjected for the detection of 18 cytokines via Th17 array. Results showed that compared with the control group, no differential expression proteins (DEPs) were found in the 1 mmol/L fluoride group; however, eight DEPs were upregulated in the 2.5 mmol/L fluoride group, including macrophage inflammatory protein-3 alpha (MIP-3 alpha), interleukin-21 (IL-21), IL-13, IL-17F, IL-28A, transforming growth factor type beta 1 (TGF-beta 1), IL-23, and IL-17A. In addition, five DEPs (MIP-3 alpha, IL-13, IL-21, TGF-beta 1, and IL-17F) were upregulated in the 2.5 mmol/L fluoride group compared with the 1 mmol/L fluoride group. Gene ontology analysis revealed that the positive regulation of cytokine production, cytokine activity, receptor ligand activity, and cytokine receptor binding accounted for high percent of DEPs present. Kyoto Encyclopedia of Genes and Genomes analysis showed that these DEPs primarily involved 12 pathways enriched in the cytokine-cytokine receptor interaction and IL-17 signaling pathway after 2.5 mmol/L fluoride treatment. The results indicated that fluoride might induce cytotoxicity by disturbing Th17-related cytokine expression.

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