Emerging PPARγ-Independent Role of PPARγ Ligands in Lung Diseases
Figure 2
PPARγ ligands inhibit TGFβ-induced Akt phosphorylation and myofibroblast differentiation with varied potency. Primary human lung fibroblasts were treated with TGFβ (5 ng/mL), alone or in combination with three PPARγ ligands (CDDO (1 μM), 15d-PGJ2 (5 μM) and rosiglitazone (20 μM)). Protein lysates were electrophoretically separated on the same gel, and representative lanes from a single experiment are shown here. The potency of a PPARγ ligand to inhibit Akt phosphorylation corresponds to its ability to inhibit myofibroblast differentiation. While CDDO inhibits both Akt phosphorylation and αSMA potently, rosiglitazone is a weak inhibitor of both.
