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15‐Deoxy‐ Δ 12,14 ‐prostaglandin J 2 inhibitsCX3CL1/fractalkine expression in human endothelial cells
Author(s) -
Imaizumi Tadaatsu,
Matsumiya Tomoh,
Tamo Wakako,
Shibata Takeo,
Fujimoto Koji,
Kumagai Mika,
Yoshida Hidemi,
Cui XueFan,
Tanji Kunikazu,
Hatakeyama Masaharu,
Wakabayashi Koichi,
Satoh Kei
Publication year - 2002
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1046/j.1440-1711.2002.01111.x
Subject(s) - ciglitazone , chemokine , troglitazone , agonist , cytokine , receptor , chemistry , tumor necrosis factor alpha , microbiology and biotechnology , endocrinology , peroxisome proliferator activated receptor , medicine , biology , immunology
Peroxisome proliferator‐activated receptor‐γ (PPAR‐γ) is a member of nuclear hormone receptor superfamily, and is known to play a role in various biological processes including inflammatory responses and adipocyte differentiation. CX3CL1/fractalkine is a potent agonist for chemotaxis and adhesion of monocytes and lymphocytes. Endothelial cells produce fractalkine when stimulated with cytokines such as interleukin‐1 (IL‐1), tumour necrosis factor‐α and interferon‐γ (IFN‐γ). We herein report that 15‐deoxy‐n 12,14 ‐prostaglandinJ 2 (15d‐PGJ 2 ), a PPAR‐γ agonist, inhibits the expression of fractalkine induced by IFN‐γ or IL‐1β in human endothelial cells. Agonist for PPAR‐α (WY14643) or PPAR‐γ (ciglitazone) did not inhibit the cytokine‐inducedfractalkine expression, and the effect of 15d‐PGJ 2 maybe independent of PPAR. 15‐Deoxy ‐ D 12,14 prostaglandin J 2 also inhibited the adhesion of blood mononuclear cells to endothelial monolayers treated with IFN‐γ or IL‐1β. The data suggest that 15d‐PGJ 2 regulates inflammatory reactions, at least in part, through the inhibition of fractalkine expression and leucocyte traffic through the endothelium.