Objective      To observe the effect of peroxisome proliferator-activated receptor-γ (PPARγ) activation on the invasive capacity of endothelial progenitor cells (EPCs) and explore the underlying mechanism.       Methods      The rat bone marrow-derived EPCs isolated and cultured in vitro were treated with PPARγ agonist rosiglitazone (0

1

5

and 10 μmol/L)

PPARγ antagonist GW9662 (5 μmol/L) or cathepsin L inhibitor Z-FF-FMK (10 μmol/L). The invasive capacity of EPCs was evaluated by Matrigel invasion assay. The mRNA and protein expression of cathepsin L were analyzed by semi-quantitative RT-PCR and Western blotting.       Results      Treatment of PPARγ agonist rosiglitazone increased the invasive capacity of EPCs in a dose-dependent manner (P0.05

P0.01). The mRNA and protein expression of cathepsin L were up-regulated by rosiglitazone in a concentration-dependent manner (P0.05

P0.01)

which was blocked by PPARγ antagonist GW9662 (5 μmol/L) (P0.01). In addition

pretreatment of EPCs with GW9662 (5 μmol/L) or cathepsin L inhibitor Z-FF-FMK (10 μmol/L) attenuated rosiglitazone-promoted EPCs invasion (P0.01).       Conclusion      These findings demonstrate that the activation of PPARγ may enhance the invasive capacity of EPCs via up-regulating cathepsin L expression.