Figure 2: Inhibition of PATs reduces inflammatory mediator-induced endothelial cell–cell junction hyperpermeability.

(a) Time- and dose-dependent effects of 2-BP on thrombin (10 U ml⁻¹)-induced reduction in transendothelial electric resistance (TER), an indicator of cell–cell adhesive barrier function. Values at each time point were normalized to their baseline at t=0. Solid line tracing represents the mean resistance, and shadow represents standard error. Embedded graph indicates peak TER values and presented as mean±s.e.m. (n=3 independent experiments). *P<0.05. (b) Representative confocal images of the adherens junction molecule VE-cadherin (green) and nuclei (blue) 30 min after thrombin with or without pretreatment of 2-BP. Arrows point to discontinued VE-cadherin strands or intercellular gaps. Scale bars, 10 μm. (c) Quantification analysis of VE-cadherin junction discontinuity from three independent experiments, presented as mean±s.e.m. *P<0.05. (d) Histamine-induced changes in hydraulic conductivity (L_p) in intact perfused venules without or with 2-BP (given 30 min prior to histamine and continuously perfused until the end of the observation). L_p indicates venular permeability to water which transports mainly via paracellular pathway. n=number of segment measurements; values in parentheses indicate number of independent experiments. *P<0.05 versus baseline, ^#P<0.05 versus histamine+vehicle. (e) Representative confocal images of VE-cadherin (green) and nuclei (blue) 10 min after histamine in endothelial cells pre-treated with 2-BP. Arrows point to discontinued VE-cadherin strands or intercellular gaps. Scale bars=10 μm. (f) Quantification analysis of VE-cadherin junction discontinuity from three independent experiments. Data are presented as mean±s.e.m. *P<0.05.