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5. 15-Deoxy-D12,14-prostaglandin J2 inhibits CX3CL1/fractalkine expression in human endothelial cells.

Author

Imaizumi T, Matsumiya T, Tamo W, Shibata T, Fujimoto K, Kumagai M, Yoshida H, Cui XF, Tanji K, Hatakeyama M, Wakabayashi K, and Satoh K

Subjects
Cell Adhesion physiology, Chemokine CX3CL1, Chemokines, CX3C biosynthesis, Cycloheximide metabolism, Humans, Interferon-gamma metabolism, Interleukin-1 metabolism, Leukocytes, Mononuclear metabolism, Membrane Proteins biosynthesis, Prostaglandin D2 analogs & derivatives, Receptors, Cytoplasmic and Nuclear agonists, Transcription Factors agonists, Umbilical Veins metabolism, Chemokines, CX3C genetics, Endothelium, Vascular metabolism, Gene Expression Regulation physiology, Membrane Proteins genetics, Prostaglandin D2 metabolism
Abstract

Peroxisome proliferator-activated receptor-gamma (PPAR-gamma)is a member of nuclear hormone receptor superfamily, and is knownto play a role in various biological processes including inflammatoryresponses and adipocyte differentiation. CX3CL1/fractalkineis a potent agonist for chemotaxis and adhesion of monocytes and lymphocytes. Endothelial cells produce fractalkine when stimulated with cytokinessuch as interleukin-1 (IL-1), tumour necrosis factor-alpha andinterferon-gamma (IFN-gamma). We herein report that 15-deoxy-n12,14 -prostaglandinJ2 (15d-PGJ2), a PPAR-gamma agonist,inhibits the expression of fractalkine induced by IFN-gamma orIL-1beta in human endothelial cells. Agonist for PPAR-alpha (WY14643)or PPAR-gamma (ciglitazone) did not inhibit the cytokine-inducedfractalkine expression, and the effect of 15d-PGJ2 maybe independent of PPAR. 15-Deoxy-D12,14 prostaglandinJ2 also inhibited the adhesion of blood mononuclear cellsto endothelial monolayers treated with IFN-gamma or IL-1beta. The data suggest that 15d-PGJ2 regulates inflammatoryreactions, at least in part, through the inhibition of fractalkineexpression and leucocyte traffic through the endothelium.

Published
2002
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