Figure 4.

Influence of Ado uptake inhibition on endothelial barrier function in vitro. (a) Indicated concentrations of Ado were added to the apical surface of normoxic (48 h, pO₂ 147) or posthypoxic (48 h, pO₂ 20 torr) HMEC-1 and permeability to FITC-dextran (70kD) was quantified. Data are derived from six monolayers in each condition and expressed as mean ± SD of percent control flux. *, significant differences from baseline (P < 0.05); ^#, differences from baseline and from normoxia (P < 0.05). (b) Influence of 10 μM dipyridamole on Ado barrier responses in normoxic and posthypoxic endothelia. (c) Influence of ENT1 and ENT2 (d) suppression by siRNA on Ado elicited endothelial barrier responses. HMEC-1 cells were loaded with ENT1- or ENT2-specific siRNA or control ribonucleotide (200 nM) and, after 48 h, permeability to 70 kD FITC was measured in the presence of indicated Ado concentrations. Data are derived from six monolayers in each condition and expressed as mean ± SD of percent control flux.