Figure 4.

Endogenous Δ¹²-PGJ₂and 15d-PGJ₂concentrations are affected when PPARγ is targeted in CML mice. Lipid extracts from the serum of BCR-ABL mice were analyzed by LC-MS/MS for Δ¹²-PGJ₂, 15d-PGJ₂, and 13,14-dihydro-15-keto PGJ₂ (13,14di-15k-PGJ₂). (A) Se-S BCR-ABL mice treated with or without GW9662. Se-S mice were given daily i.p. injection of GW9662 (1 mg/kg) starting 1 day prior to BCR-ABL transplant until euthanized (n = 3). (B) Pioglitazone (5 mg/kg) was given by i.p. injection daily starting 1 day prior to BCR-ABL transplant (n = 5-6). Bars represent biological mean ± SEM (*P < .05). (C) Schematic of selenium supplementation and GW9662 involvement in endogenous PPARγ ligand synthesis in BCR-ABL mice. Se-S diet increases H-Pgds, leading to subsequent increase in Δ¹²-PGJ₂ and 15d-PGJ₂. Pioglitazone may also increase CyPGs. GW9662 in Se-S BCR-ABL mice increases 15-Pgdh, which leads to breakdown of Δ¹²-PGJ₂ and 15d-PGJ₂.