Prostaglandin J2 series induces the gene expression of monocyte chemoattractant protein-1 during the maturation phase of cultured adipocytes.

Prostaglandin (PG) J(2) series including Δ(12)-PGJ(2) and 15-deoxy-Δ(12,14)-prostaglandin J(2) (15d-PGJ(2)) is the dehydration products of PGD(2) that are biosynthesized through the cyclooxygenase (COX) pathway. These prostanoids are active ligands for peroxisome proliferator-activated receptor γ (PPARγ), a master regulator of adipogenesis in adipocytes. Here we investigated whether PGJ(2) derivatives can modulate the gene expression of monocyte chemoattractant protein-1 (MCP-1), a pro-inflammatory chemokine, during the maturation phase of adipocytes. Each of selective or nonselective inhibitors for COX isoforms suppressed significantly the accumulation of fats by interfering the induced expression of the PPARγ gene. Immunological assays of PGJ(2) series revealed higher production of Δ(12)-PGJ(2) than 15d-PGJ(2) by cultured adipocytes, implicating the contribution of endogenous PGJ(2) series to the stimulated adipogenesis. In addition, the increased transcription of MCP-1 was detectable at later maturation phase of adipogenesis, which was prevented by co-incubation with aspirin. Although 15d-PGJ(2) was more potent than Δ(12)-PGJ(2), both PGJ(2) derivatives series had similar effects to rescue dose-dependently the expression of the MCP-1 gene attenuated by aspirin. These findings suggest that the expression of MCP-1 involved in adipocyte inflammation could be positively regulated by the PGJ(2) series during adipogenesis in adipose tissue.