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. Author manuscript; available in PMC: 2017 Mar 15.
Published in final edited form as: Circulation. 2016 Feb 2;133(11):1093–1103. doi: 10.1161/CIRCULATIONAHA.115.020918

Figure 7.

Figure 7

Reduced expression of p110γ in pulmonary vascular endothelial cells of ARDS patients. (A–C) Normalization of vascular repair and improved survival of Pik3cg−/−/Tg mice following CLP sepsis. EBA extravasation demonstrating defective vascular repair in Pik3cg−/− lungs following CLP sepsis, which was rescued by overexpression of FoxM1 in Pg−/−/Tg mouse lungs (A). Time course of lung tissue MPO activity (B). *, P < 0.01 (ANOVA). Improved survival of Pg−/−/Tg mice (C). Mortality rate was monitored for 5 days following CLP. Approximately 60% of the Pik3cg−/− mice died within 72h post-CLP. *, P < 0.01 (Mantel-Cox). (D) Representative micrographs of immunostaining demonstrating diminished expression of p110γ in pulmonary vascular ECs of ARDS patients. Arrows, ECs expressing p110γ. Scale bar, 40 μm. V, vessel. (E) Quantification of p110γ expression in pulmonary vascular ECs of human lung samples. The fluorescence intensity of p110γ staining in pulmonary vascular ECs was scored from 1 to 5, with 5 as the highest. *, P = 0. 01 (Mann-Whitney). A.U, arbitrary units.