Fig. 6.

Akt but not NOS3 is critical for restoration of H₂O₂-perturbed HCMVEC monolayer integrity. HCMVEC were grown on gold electrical cell substrate impedance sensing electrodes, and transendothelial cell electrical resistance (TEER) was recorded as described in materials and methods. A: dose dependency of H₂O₂-induced permeability. B: Akt is critical for restoration of H₂O₂-elicited permeability. HCMVEC were pretreated with 10 μM Akt inhibitor API-2 for 2 h and then stimulated with 250 μM H₂O₂. Note that API-2 alone has no effect on HCMVEC TEER measures during baseline conditions. C: NO synthases downstream of Akt do not mediate the H₂O₂-induced permeability dynamic in HCMVEC. HCMVEC were pretreated with 200 μM l-NAME for 2 h and then stimulated with 250 or 500 μM H₂O₂. Note that l-NAME alone has no effect of HCMVEC TEER dynamic. Data represent means ± SE of 4 independent experiments.