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. 2016 May 4;11(5):e0154720. doi: 10.1371/journal.pone.0154720

Fig 2. PPARγ inhibited PDGF-BB-induced VSMC proliferation, migration and oxidative stress.

Fig 2

Cultured VSMCs were incubated with RSG (10μmol/L) for different times (0, 1, 6, 12 or 24 h). PPARγ expression increased in time-dependent manner, with an obvious effect at 6 h and the peak at 12 h that sustained after 24 h (a). (*P<0.05 vs. 0 h). RSG treatment for 12 h significantly counteracted ROS generation induced by PDGF-BB in VSMCs, while PPARγ inhibitor GW9662 diminished the effect of RSG (b). VSMCs treated with RSG showed reduced proliferation and PCNA expression, VSMC migration and MMP9 expression in response to PDGF-BB, which was reversed by GW9662 (c and d). (*P<0.05 vs. con; #P<0.05 vs. PDGF; ΔP<0.05 vs. PDGF+RSG). Con, wild-type VSMCs in basal conditions; PDGF, PDGF-BB, platelet derived growth factor-BB; ROS, reactive oxygen species; RSG, rosiglitazone; GW9662, PPARγ inhibitor; PCNA, proliferating cell nuclear antigen; MMP9, matrix metalloproteinase 9.