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. 2013 Apr 2;288(21):15380–15389. doi: 10.1074/jbc.M112.427765

FIGURE 6.

FIGURE 6.

Endomembrane H-Ras activates •NO production by activating the PI3K/Akt/eNOS signaling cascade. A, H-Ras-mediated EC migration was inhibited by inhibition of PI3K. H-Ras depleted and reconstituted with either LacZ, H-Ras WT, or H-Ras PalM HAECs were stimulated with VEGF (50 ng/ml), and an EC wound healing assay was performed. ECs were treated with either DMSO or the PI3K inhibitor LY294002 (5 μm) during migration. One-way ANOVA and Dunnett's post-test were used (n ≥ 4). Error bars, S.E. **, p < 0.01, treatment versus no treatment; *, p < 0.05, reconstitution with LacZ versus H-Ras WT or PalM. B, H-Ras-mediated EC migration was reduced by inhibiting eNOS with l-NAME. The wound healing assay was performed as described above, and cells were treated with l-NAME (1 mm) for the duration of the assay. Unpaired Student's t test was used (n ≥ 3). Error bars, S.E. **, p < 0.01; *, p < 0.05, treatment versus no treatment. C, H-Ras-mediated proangiogenic signaling was reduced by inhibition of PI3K. H-Ras-depleted and -reconstituted HAECs were preincubated with LY294002 (10 μm) and then stimulated with VEGF (50 ng/ml, 30 min). A representative Western blot is shown.