Requirement of FoxM1 for reforming a restrictive barrier in ECs after PAR-1 activation. (A) TER assay of endothelial AJ integrity in response to thrombin challenge (PAR-1 activation). HMVEC-L transfected with either human FoxM1 siRNA (siRNA) or scRNA, or mock-transfected (CTL), were plated to confluency on electrodes. AT 65 h after transfection, TER of each monolayer at baseline was recorded, and it was then monitored for 3 h after thrombin challenge (4 U/ml). TER values of each monolayer were normalized to their values at basal levels. Data are expressed as mean ± SD (error bars; n = 3 independent experiments). *, P < 0.05 versus either CTL or scRNA. FoxM1 deficiency induced a defective recovery of the endothelial barrier function after thrombin challenge. (B) Western blot analysis demonstrating siRNA-mediated knockdown of FoxM1 in HMVEC-L. At 65 h after transfection, HMVEC-L were lysed, and 15 µg of each lysate per lane was loaded for detection of FoxM1 protein level with anti-FoxM1 antibody. The same membrane was blotted with anti-actin antibody for loading control. The experiment was performed three times with similar results.