Skip to main content
. Author manuscript; available in PMC: 2011 Oct 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2010 Jul 22;30(10):1952–1959. doi: 10.1161/ATVBAHA.110.211474

Figure 3.

Figure 3

KLF2 deficiency increases endothelial leakage. (A) KLF2 deficiency in HUVEC lead to an enhancement of inter-endothelial gap formation response to thrombin treatment. HUVEC were transfected with control siRNA and KLF2 siRNA, five days after transfection, cells were treated with thrombin (1U/ml) for gap formation assessment by actin staining. Percentage of exposed areas was quantified by NIH Image J software. The control group (NS with thrombin) was normalized to 100%. A representative of three independent experiments is shown. Scale bar, 50 μm. (B) Deficiency of KLF2 lead to increased endothelial leakage in response to thrombin. HUVEC were transfected with control siRNA and KLF2 siRNA for two days, then cells were replated onto transwell; permeability analysis was performed following treatment with thrombin. N=6, p<0.01. (C) KLF2 deficiency leads to increased endothelial leakage in response to hydrogen peroxide. HUVEC were transfected as above, and treated with hydrogen peroxide (200uM) followed by permeability assay. N=6, p<0.01. (D) Partial deficiency of KLF2 in primary ECs lead to a significant increase of endothelial leakage when treated with thrombin. Confluent lung microvascular endothelial cells from KLF2+/+ and KLF2+/− mice were treated with thrombin, then permeability assay performed. N=6, p<0.01.