Figure 1. Expression and phosphorylation state of Akt, ERK-1/-2, MAP kinase/p38, and JNK-1/-2 in WT and V1tg mice subjected to focal cerebral ischemia. Animals were either untreated or i.c.v. treated with 2 µl of the solvent DMSO or DMSO containing Wortmannin, a PI3K/Akt inhibitor. Tissue samples were taken from the ischemic cortex and underlying striatum. Note that human VEGF increases phosphorylated (but not total) Akt and ERK-1/-2 and reduces phosphorylated p38 and JNK-1/-2 levels. Furthermore, note the reversal of p38, but not of ERK-1/-2 or JNK-1/-2 phosphorylation in animals treated with Wortmannin, in which Akt phosphorylation was suppressed. Our data suggested that Akt was involved in VEGF’s neuroprotective function and BBB permeability. Values are mean ± SD (n=3 samples/group), normalized with corresponding blots for ß-actin. *P < 0.05 compared with WT mice; ^#P < 0.05 compared with V1tg mice receiving DMSO.