Figure 5. Rescue of defective reannealing of endothelial AJ barrier of FoxM1-deficient ECs by restoration of β-catenin protein. (A and B) Decreased β-catenin expression is responsible for impaired reannealing of the endothelial AJ barrier in FoxM1-deficient HMVEC-L. HMVEC-L were transfected with human FoxM1 scRNA, siRNA, and siRNA plus plasmid DNA expressing human β-catenin (siRNA+β-cat). At 65 h after transfection, the monolayers were challenged with 4 U/ml thrombin, and TER was recorded for 3 h. Data are expressed as mean ± SD (error bars; n = 3 independent experiments). *, P < 0.05 versus scRNA. (C and D) β-catenin expression rescued defective reannealing of the endothelial AJ barrier of FoxM1-deficient HMVEC-L in a dose-dependent manner. HMVEC-L were transfected with either FoxM1 scRNA, siRNA, or siRNA plus plasmid DNA expressing human β-catenin at the indicated amounts. At 65 h after transfection, monolayers were challenged with 4 U/ml thrombin, and TER was recorded for 3 h. Data are expressed as mean ± SD (error bars; n = 3 independent experiments). *, P < 0.05 versus scRNA. (E) Western blots demonstrating increased β-catenin expression in FoxM1-deficient HMVEC-L by plasmid DNA transfection. The experiment was performed three times with similar results.
Figure 5.

Rescue of defective reannealing of endothelial AJ barrier of FoxM1-deficient ECs by restoration of β-catenin protein. (A and B) Decreased β-catenin expression is responsible for impaired reannealing of the endothelial AJ barrier in FoxM1-deficient HMVEC-L. HMVEC-L were transfected with human FoxM1 scRNA, siRNA, and siRNA plus plasmid DNA expressing human β-catenin (siRNA+β-cat). At 65 h after transfection, the monolayers were challenged with 4 U/ml thrombin, and TER was recorded for 3 h. Data are expressed as mean ± SD (error bars; n = 3 independent experiments). *, P < 0.05 versus scRNA. (C and D) β-catenin expression rescued defective reannealing of the endothelial AJ barrier of FoxM1-deficient HMVEC-L in a dose-dependent manner. HMVEC-L were transfected with either FoxM1 scRNA, siRNA, or siRNA plus plasmid DNA expressing human β-catenin at the indicated amounts. At 65 h after transfection, monolayers were challenged with 4 U/ml thrombin, and TER was recorded for 3 h. Data are expressed as mean ± SD (error bars; n = 3 independent experiments). *, P < 0.05 versus scRNA. (E) Western blots demonstrating increased β-catenin expression in FoxM1-deficient HMVEC-L by plasmid DNA transfection. The experiment was performed three times with similar results.

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