Figure 1
Figure 1. Ang-1 stimulation counteracts VEGF-induced transendothelial permeability and NO production. (A) Transendothelial permeability was determined by measuring the passage of FITC-dextran through a monolayer of BAEC. Passage of FITC-dextran was measured after exposure of BAEC to VEGF, Ang-1, or VEGF and Ang-1 in combination (at the indicated concentrations). In some cases, cells were pretreated with the NOS inhibitor, l-NAME, as indicated. The data represent permeability to FITC-dextran expressed as the mean fold increases (± SEM) with respect to untreated cells. (B) NO released in the culture medium of BAEC subjected to 30-minute stimulation with Ang-1 (100 ng/mL), VEGF (40 ng/mL), or both. Samples of culture medium were taken for nitrite quantification, as described in “NO release analysis.” Data are the average ± SEM of at least 4 experiments. *P < .05.

Ang-1 stimulation counteracts VEGF-induced transendothelial permeability and NO production. (A) Transendothelial permeability was determined by measuring the passage of FITC-dextran through a monolayer of BAEC. Passage of FITC-dextran was measured after exposure of BAEC to VEGF, Ang-1, or VEGF and Ang-1 in combination (at the indicated concentrations). In some cases, cells were pretreated with the NOS inhibitor, l-NAME, as indicated. The data represent permeability to FITC-dextran expressed as the mean fold increases (± SEM) with respect to untreated cells. (B) NO released in the culture medium of BAEC subjected to 30-minute stimulation with Ang-1 (100 ng/mL), VEGF (40 ng/mL), or both. Samples of culture medium were taken for nitrite quantification, as described in “NO release analysis.” Data are the average ± SEM of at least 4 experiments. *P < .05.

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