Abstract
Retinoic acid-inducible gene-I (RIG-I) is a member of the DExH box protein family and designated as a putative RNA helicase. RIG-I is implicated in host defense and inflammatory reactions by regulating the expression of various genes. RIG-I is expressed in endothelial cells and upregulated with lipopolysaccharide (LPS). Peroxisome proliferator-activated receptor-γ (PPAR-γ) is a nuclear hormone receptor and regulates gene expressions in response to its specific ligands. In the present study, we examined the effect of PPAR-γ ligands on the LPS-induced RIG-I expression in cultured human umbilical vein endothelial cells (HUVEC). 15-Deoxy-Δ 12,14-prostaglandin J 2 (15d-PGJ 2), a metabolite of PGD 2, is a natural ligand for PPAR-γ and known to modulate inflammatory reactions by regulating the expression of various genes in PPAR-γ-dependent and -independent manners. LPS-induced RIG-I expression in HUVEC was inhibited by pretreatment of the cells with 15d-PGJ 2 in time-and concentration-dependent manners. However, ciglitazone and bisphenol A diglycide ether, authentic and specific ligands for PPAR-γ, did not affect the RIG-I expression. These results suggest that 15d-PGJ 2 inhibits LPS-induced RIG-I expression through a mechanism independent on PPAR-γ. 15d-PGJ 2 may regulate inflammatory reactions, at least in part, by inhibiting the expression of RIG-I.
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