We studied the effect of peroxisome proliferator-activated receptor γ (PPARγ) activation on thromboxane A2(TXA2) and prostaglandin E2(PGE2) production in monocyte/macrophage cell lines. In present experiment, we used human peripheral blood monocyte (PBMC), monocyte-cell line THP-1 and mouse macrophage-like cell line RAW264.7. The expression of PPARγ is reported in PBMC and THP-1. Synthetic PPARγ ligands (troglitazone or BRL49653) inhibited TXA2 production and enhanced PGE2 production of PBMC and THP-1. When treated with 0.5-10 μM of troglitazone, there were no significant changes of TXA2 and PGE2 production of RAW264.7 cells, which express very low levels of PPARγ. When RAW264.7 cells was transfected with PPARγ expression plasmid and treated with troglitazone, PPARγ was activated in a dose-dependent manner. In PPARγ-transfected RAW264.7, TXA2 production was decreased and PGE2 production was increased by troglitazone treatment. But it needs high concentration of troglitazone (10 μM) for increasing PGE2 production. These results suggest that PPARγ may have negative effect on TXA2 production, and also have slightly positive effect on PGE2 production of macrophage.
|Number of pages||7|
|Journal||Prostaglandins Leukotrienes and Essential Fatty Acids|
|Publication status||Published - 2002 Jan 1|
ASJC Scopus subject areas
- Clinical Biochemistry
- Cell Biology