Figure 2.

Impairment of vascular repair in Pik3cg^−/− mice secondary to inhibition of FoxM1 expression. (A) Pulmonary transvascular EBA flux demonstrating defective vascular repair in Pik3cg^−/− mouse lungs which was rescued by overexpression of FoxM1 in Pg^−/−/Tg mice. n = 5. *, P < 0.05; *, P < 0.01 (ANOVA). (B) Scanning electron microscopy demonstrating p110γ-mediated FoxM1 expression is required for vascular repair. Representative micrographs of lung sections from mice challenged with LPS for 60h are shown. Pik3cg^−/− mouse lungs had extensive extravasation (Ex) of methacrylate tracer on the cut surfaces and many alveoli were filled with the tracer. However, Pg^−/−/Tg lungs displayed normal profile similar to WT lungs. A, airways. The experiment was performed 3 times with similar data. Scale bar, 20μm. (C) Representative Western blotting of p110γ and FoxM1 in lung lysates at basal. Experiment were performed three times with similar results. (D) Representative micrographs of cremaster muscle venule demonstrating marked leakage of FITC-conjugated dextran in Pik3cg^−/− mice in contrast to WT and Pg^−/−/Tg at 48h post-LPS. Thirty min post-administration of FITC-conjugated dextran (i.v.), vascular permeability in the cremaster muscle venule was monitored by the FITC signal in an area of 0.02 mm². The vessel walls were indicated in white lines. Scale bar, 10μm. (E) Graphic presentation of prominent vascular leakiness in Pik3cg^−/− mice at 48h post-LPS challenge, which was rescued by FoxM1 overexpression in Pg^−/−/Tg mice. n = 6 venules in 3 mice/group. *, P < 0.0001 (ANOVA).