Fig. 4.
Fig. 4. Effect of pharmacologic inhibitors of PKC, p38 and p42/44 MAPK, and NF-κB on thrombin-induced DAF. / HUVEC monolayers were preincubated with (A) the PKC inhibitor RO31-8220 (1 μmol/L), (B) the p38 inhibitor SB202190 (25 μmol/L), (C) the MEK-1 inhibitor of p42/44 MAPK phosphorylation PD98059 (50 μmol/L), or (D) the NF-κB inhibitor PSI (10 μmol/L) for 1 hour prior to the addition of 10 U/mL thrombin for 24 hours. The ECs were then harvested and stained with MoAb to DAF (1H4) for analysis by flow cytometry. The data are expressed as a percentage of the DAF expression on thrombin-treated cells and are presented as the mean ± SEM of 3 experiments performed on separate HUVEC cultures.

Effect of pharmacologic inhibitors of PKC, p38 and p42/44 MAPK, and NF-κB on thrombin-induced DAF.

HUVEC monolayers were preincubated with (A) the PKC inhibitor RO31-8220 (1 μmol/L), (B) the p38 inhibitor SB202190 (25 μmol/L), (C) the MEK-1 inhibitor of p42/44 MAPK phosphorylation PD98059 (50 μmol/L), or (D) the NF-κB inhibitor PSI (10 μmol/L) for 1 hour prior to the addition of 10 U/mL thrombin for 24 hours. The ECs were then harvested and stained with MoAb to DAF (1H4) for analysis by flow cytometry. The data are expressed as a percentage of the DAF expression on thrombin-treated cells and are presented as the mean ± SEM of 3 experiments performed on separate HUVEC cultures.

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