Ciglitazone inhibits the antigen-induced leukotrienes production independently of PPARγ in RBL-2H3 mast cells

Peroxisome prolifelator-activated receptor γ (PPARγ) is a ligand-activated transcription factor, through which PPARγ agonists have been demonstrated to down-regulate inflammatory cell functions. Recently, the agonists are reported to exert, in some conditions, their inhibitory actions independently of PPARγ. Previously, we showed that a PPARγ agonist, troglitazone, inhibited cycteinyl (Cys)-leukotrienes production in RBL-2H3 cells after IgE receptor triggering. Here we examined whether the inhibition of cycteinyl-leukotrienes production in the cells was dependent on the activation of PPARγ. A PPARγ agonist, ciglitazone, significantly inhibited Cys-leukotrienes, but not prostaglandin D2, production. The inhibition was not attenuated by the pretreatment with a PPARγ antagonist. Ciglitazone did not alter the mRNA expression of acyl-coenzyme A binding protein, the gene expression of which is up-regulated by PPARγ, nor induce the nucleus translocation of PPARγ. These results suggest that the inhibition by PPARγ agonists of Cys-leukotrienes production in RBL-2H3 cells after IgE receptor triggering is not through the activation of PPARγ.