Expression and function of the P2Y14 receptor in murine peritoneal macrophages

DOI IR HANDLE Web Site
  • Kudo Fujimi
    Department of Biomedical Sciences, Hirosaki University Graduate School of Health Sciences
  • Nishiguchi Naoki
    R&D Center, Sekisui Chemical Co., Ltd.
  • Ito Kyoko
    Department of Biomedical Sciences, Hirosaki University Graduate School of Health Sciences
  • Nakano Manabu
    Department of Biomedical Sciences, Hirosaki University Graduate School of Health Sciences Research Center for Biomedical Sciences, Hirosaki University Graduate School of Health Sciences
  • Ito Koichi
    Department of Biomedical Sciences, Hirosaki University Graduate School of Health Sciences Research Center for Biomedical Sciences, Hirosaki University Graduate School of Health Sciences

Bibliographic Information

Other Title
  • マウス腹腔マクロファージにおける P2Y14受容体の発現と機能

Search this article

Abstract

    The P2Y14 receptor is activated by UDP-glucose (UDPG), which is a well-known glycosyl donor that participates in the biosynthesis of carbohydrates, and is widely expressed in immune cells. During inflammation and mechanical stress, damaged cells release nucleotides, including ATP and UDPG, as danger signals that act as P2Y receptor agonists. These nucleotide-induced signals participate in the regulation of immune responses. In this study, to investigate P2Y14 expression further, we performed flow cytometric analysis using an anti-P2Y14 monoclonal antibody. The results indicated that P2Y14 is expressed in murine immune cells, including T cells, B cells, monocytes, granulocytes, and CD11bhigh macrophages. Interestingly, the expression levels of P2Y14 differed between immature and mature monocytes, and in CD11bhigh macrophages, P2Y14 was gradually downregulated as peritonitis was terminated. The expression of CD11b is reduced by the efferocytosis of apoptotic neutrophils during peritonitis, and the induced CD11blow macrophages, which emerge in the resolution of peritonitis, play an important role in the termination of inflammation. Consistent with this observation, we revealed that administration of UDPG to mice with induced peritonitis increased the number of CD11blow macrophages. As P2Y14 is expressed in CD11bhigh macrophages but not in CD11blow macrophages, UDPG may participate in the conversion to the CD11blow phenotype. These data suggest a novel regulatory pathway of the inflammatory response via P2Y14 expressed on macrophages.

Journal

  • Hirosaki Medical Journal

    Hirosaki Medical Journal 63 (2-4), 96-104, 2012

    Hirosaki University Graduate School of Medicine,Hirosaki Medical Society

Keywords

Details 詳細情報について

Report a problem

Back to top