In:
Immunology & Cell Biology, Wiley, Vol. 80, No. 6 ( 2002-12), p. 531-536
Abstract:
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.
Type of Medium:
Online Resource
ISSN:
0818-9641
,
1440-1711
DOI:
10.1046/j.1440-1711.2002.01111.x
Language:
English
Publisher:
Wiley
Publication Date:
2002
detail.hit.zdb_id:
2011707-3
SSG:
12