Figure 5
Figure 5. Induction of permeability by Sema3A is Src independent, but is blocked by PI3Kγ/δ inhibition. (A) Treatment with the Src family kinase inhibitor SKI-606 (5 mg/kg intraperitoneally) prior to injection with Sema3A, VEGF, or PBS significantly inhibits VEGF- but not Sema3A-mediated VP (n = 10, *P < .05). (B) Yes+/+ and Yes−/− mice show similar VP response when injected with Sema3A or PBS (n = 8). (C) Sema3A- and VEGF-induced VP depends on PI3Kγ/δ as determined by treatment of mice with the PI3Kγ/δ inhibitor TG100–115 (5 mg/kg intraperitoneally) prior to injection with Sema3A, VEGF, or PBS (n = 5, *P < .05, **P < .01). Error bars represent SEM.

Induction of permeability by Sema3A is Src independent, but is blocked by PI3Kγ/δ inhibition. (A) Treatment with the Src family kinase inhibitor SKI-606 (5 mg/kg intraperitoneally) prior to injection with Sema3A, VEGF, or PBS significantly inhibits VEGF- but not Sema3A-mediated VP (n = 10, *P < .05). (B) Yes+/+ and Yes−/− mice show similar VP response when injected with Sema3A or PBS (n = 8). (C) Sema3A- and VEGF-induced VP depends on PI3Kγ/δ as determined by treatment of mice with the PI3Kγ/δ inhibitor TG100–115 (5 mg/kg intraperitoneally) prior to injection with Sema3A, VEGF, or PBS (n = 5, *P < .05, **P < .01). Error bars represent SEM.

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