Fig. 2

Bevacizumab promotes venous thrombosis in a PAI-1-dependent manner. a. The intrathrombotic gene expression of PAI-1 in the bevacizumab and vehicle groups was determined via real-time RT-PCR. All values represent mean ± SEM (n = 6/group). *P < 0.01 vs. the vehicle group. b. IVC stenosis was induced in WT and Pai-1 ^−/− mice (n = 6/group). Ten days after ligation, all mice were euthanized, and the weight of the thrombus was determined. *P < 0.05 vs. the vehicle group in WT mice; **P < 0.05 vs. the vehicle group in WT mice; ^#P < 0.05 vs. the bevacizumab group in WT mice, and ^#P = 0.74 vs. the vehicle group in Pai-1 ^−/− mice (n = 6/group). c. Saphenous vein thrombosis was induced using 10 % FeCl3 in WT and Pai-1 ^−/− mice (n = 6/group). Occlusion times were measured and are shown as the mean ± SEM. *P < 0.05 vs. the vehicle group in WT mice; **P < 0.05 vs. the vehicle group in WT mice; ^#P < 0.05 vs. the bevacizumab group in WT mice. d. A549 cells were cultured for 24 hrs in the presence and absence of VEGF (50 ng/mL) and bevacizumab (250 μg/mL), as indicated. Cell lysates were prepared and subjected to Western blotting to detect PAI-1and β-actin. Representative blot and densitometric analyses of 3 independent experiments are shown. *P < 0.05 vs. control (i.e. no VEGF or Beva)