Peroxisome proliferator-activated receptor ligands negatively regulate the expression of the high-affinity IgE receptor FcεRI in human basophilic KU812 cells

Yoshinori Fujimura, Hirofumi Tachibana, Koji Yamada

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18 Citations (Scopus)

Abstract

The high-affinity IgE receptor FcεRI is expressed on the cell surface of mast cells and basophils, and plays a central role in IgE-mediated inflammatory reactions. Recently, peroxisome proliferator-activated receptors (PPARs) have been implicated in the anti-inflammatory response. To investigate a possible role for PPAR in human basophils, the effect of PPAR ligands on FcεRI expression in human basophilic KU812 cells was studied. The PPARα ligand, leukotriene B4, did not affect the cell surface expression of FcεRI. However, prostaglandin (PG) A1 and 15-deoxy-Δ12,14 PGJ2 (15d-PGJ2), which are PPARβ and γ ligands, respectively, were both able to decrease FcεRI expression. Treatment with PGA1 or 15d-PGJ2 separately also reduced histamine release from KU812 cells in response to cross-linkage of FcεRI. In addition, RT-PCR analysis showed that KU812 cells expressed the mRNA for PPARα, β, and γ, indicating that PPARβ or γ may negatively regulate the cell activation via FcεRI. Cells treated with 15d-PGJ2 expressed lower levels of FcεRIα and γ mRNA, and PGA1 treatment decreased the level of FcεRIγ mRNA. These results suggest that the suppression of FcεRI expression by PPARs may be due to the down-regulation of FcεRIα or γ mRNA.

Original languageEnglish
Pages (from-to)193-201
Number of pages9
JournalBiochemical and Biophysical Research Communications
Volume297
Issue number2
DOIs
Publication statusPublished - Nov 6 2002

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IgE Receptors
Peroxisome Proliferator-Activated Receptors
Ligands
Messenger RNA
Basophils
Leukotriene B4
Histamine Release
Mast Cells
Immunoglobulin E
Histamine
Anti-Inflammatory Agents
Down-Regulation
Chemical activation
Polymerase Chain Reaction

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

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title = "Peroxisome proliferator-activated receptor ligands negatively regulate the expression of the high-affinity IgE receptor FcεRI in human basophilic KU812 cells",
abstract = "The high-affinity IgE receptor FcεRI is expressed on the cell surface of mast cells and basophils, and plays a central role in IgE-mediated inflammatory reactions. Recently, peroxisome proliferator-activated receptors (PPARs) have been implicated in the anti-inflammatory response. To investigate a possible role for PPAR in human basophils, the effect of PPAR ligands on FcεRI expression in human basophilic KU812 cells was studied. The PPARα ligand, leukotriene B4, did not affect the cell surface expression of FcεRI. However, prostaglandin (PG) A1 and 15-deoxy-Δ12,14 PGJ2 (15d-PGJ2), which are PPARβ and γ ligands, respectively, were both able to decrease FcεRI expression. Treatment with PGA1 or 15d-PGJ2 separately also reduced histamine release from KU812 cells in response to cross-linkage of FcεRI. In addition, RT-PCR analysis showed that KU812 cells expressed the mRNA for PPARα, β, and γ, indicating that PPARβ or γ may negatively regulate the cell activation via FcεRI. Cells treated with 15d-PGJ2 expressed lower levels of FcεRIα and γ mRNA, and PGA1 treatment decreased the level of FcεRIγ mRNA. These results suggest that the suppression of FcεRI expression by PPARs may be due to the down-regulation of FcεRIα or γ mRNA.",
author = "Yoshinori Fujimura and Hirofumi Tachibana and Koji Yamada",
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N2 - The high-affinity IgE receptor FcεRI is expressed on the cell surface of mast cells and basophils, and plays a central role in IgE-mediated inflammatory reactions. Recently, peroxisome proliferator-activated receptors (PPARs) have been implicated in the anti-inflammatory response. To investigate a possible role for PPAR in human basophils, the effect of PPAR ligands on FcεRI expression in human basophilic KU812 cells was studied. The PPARα ligand, leukotriene B4, did not affect the cell surface expression of FcεRI. However, prostaglandin (PG) A1 and 15-deoxy-Δ12,14 PGJ2 (15d-PGJ2), which are PPARβ and γ ligands, respectively, were both able to decrease FcεRI expression. Treatment with PGA1 or 15d-PGJ2 separately also reduced histamine release from KU812 cells in response to cross-linkage of FcεRI. In addition, RT-PCR analysis showed that KU812 cells expressed the mRNA for PPARα, β, and γ, indicating that PPARβ or γ may negatively regulate the cell activation via FcεRI. Cells treated with 15d-PGJ2 expressed lower levels of FcεRIα and γ mRNA, and PGA1 treatment decreased the level of FcεRIγ mRNA. These results suggest that the suppression of FcεRI expression by PPARs may be due to the down-regulation of FcεRIα or γ mRNA.

AB - The high-affinity IgE receptor FcεRI is expressed on the cell surface of mast cells and basophils, and plays a central role in IgE-mediated inflammatory reactions. Recently, peroxisome proliferator-activated receptors (PPARs) have been implicated in the anti-inflammatory response. To investigate a possible role for PPAR in human basophils, the effect of PPAR ligands on FcεRI expression in human basophilic KU812 cells was studied. The PPARα ligand, leukotriene B4, did not affect the cell surface expression of FcεRI. However, prostaglandin (PG) A1 and 15-deoxy-Δ12,14 PGJ2 (15d-PGJ2), which are PPARβ and γ ligands, respectively, were both able to decrease FcεRI expression. Treatment with PGA1 or 15d-PGJ2 separately also reduced histamine release from KU812 cells in response to cross-linkage of FcεRI. In addition, RT-PCR analysis showed that KU812 cells expressed the mRNA for PPARα, β, and γ, indicating that PPARβ or γ may negatively regulate the cell activation via FcεRI. Cells treated with 15d-PGJ2 expressed lower levels of FcεRIα and γ mRNA, and PGA1 treatment decreased the level of FcεRIγ mRNA. These results suggest that the suppression of FcεRI expression by PPARs may be due to the down-regulation of FcεRIα or γ mRNA.

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