Rosiglitazone Regulates Anti-Inflammation and Growth Inhibition via PTEN
Figure 9
A schematic model of the anti-inflammatory and growth inhibitory effects of rosiglitazone in PTEN-deficient RAW 264.7 cells. Lower doses (<25 M) of rosiglitazone inhibited LPS-induced NO release, PGE2 production, and activation of Akt in RAW 264.7 murine macrophages. These anti-inflammatory effects of rosiglitazone were dependent on PTEN, but they did not affect the production of ROS. In addition to a significantly higher inflammatory response and elevated production of ROS, PTEN knockdown caused increased cell growth and altered signaling molecule expression including Akt, p38 MAPK, and ERK. On the other hand, higher doses (<100 M) of rosiglitazone delayed cell growth inhibition in PTEN-deficient cells through inhibition of ROS production and p38 MAPK activation.
