| Literature DB >> 12406386 |
Tadaatsu Imaizumi1, Tomoh Matsumiya, Wakako Tamo, Takeo Shibata, Koji Fujimoto, Mika Kumagai, Hidemi Yoshida, Xue-Fan Cui, Kunikazu Tanji, Masaharu Hatakeyama, Koichi Wakabayashi, Kei Satoh.
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.Entities:
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Year: 2002 PMID： 12406386 DOI： 10.1046/j.1440-1711.2002.01111.x
Source DB: PubMed Journal: Immunol Cell Biol ISSN： 0818-9641 Impact factor: 5.126