Expression of Fgf23 in Activated Dendritic Cells and Macrophages in Response to Immunological Stimuli in Mice

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  • Masuda Yuki
    Department of Microbial Chemistry, Kobe Pharmaceutical University
  • Ohta Hiroya
    Department of Genetic Biochemistry, Kyoto University Graduate School of Pharmaceutical Sciences
  • Morita Yumiko
    Department of Microbial Chemistry, Kobe Pharmaceutical University
  • Nakayama Yoshiaki
    Department of Microbial Chemistry, Kobe Pharmaceutical University
  • Miyake Ayumi
    Department of Genetic Biochemistry, Kyoto University Graduate School of Pharmaceutical Sciences
  • Itoh Nobuyuki
    Department of Genetic Biochemistry, Kyoto University Graduate School of Pharmaceutical Sciences
  • Konishi Morichika
    Department of Microbial Chemistry, Kobe Pharmaceutical University

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Fibroblast growth factors (Fgfs) are polypeptide growth factors with diverse biological activities. While several studies have revealed that Fgf23 plays important roles in the regulation of phosphate and vitamin D metabolism, the additional physiological roles of Fgf23 remain unclear. Although it is believed that osteoblasts/osteocytes are the main sources of Fgf23, we previously found that Fgf23 mRNA is also expressed in the mouse thymus, suggesting that it might be involved in the immune system. In this study we examined the potential roles of Fgf23 in immunological responses. Mouse serum Fgf23 levels were significantly increased following inoculation with Escherichia coli or Staphylococcus aureus or intraperitoneal injection of lipopolysaccharide. We also identified activated dendritic cells and macrophages that potentially contributed to increased serum Fgf23 levels. Nuclear factor-kappa B (NF-κB) signaling was essential for the induction of Fgf23 expression in dendritic cells in response to immunological stimuli. Moreover, we examined the effects of recombinant Fgf23 protein on immune cells in vitro. Fgfr1c, a potential receptor for Fgf23, was abundantly expressed in macrophages, suggesting that Fgf23 might be involved in signal transduction in these cells. Our data suggest that Fgf23 potentially increases the number in macrophages and induces expression of tumor necrosis factor-α (TNF-α), a proinflammatory cytokine. Collectively, these data suggest that Fgf23 might be intimately involved in inflammatory processes.

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