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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 6.

Figure 6

Endothelial expression of FoxM1 rescued the defective vascular repair phenotype of Pik3cg−/− mouse lungs. (A) QRT-PCR analysis demonstrating restored expression of FoxM1 in Pik3cg−/− mouse lungs. At 12h post-LPS, plasmid DNA expressing human FOXM1 under control of the CDH5 promoter (FOXM1) or empty vector was transduced in Pik3cg−/− lungs. At 60h post-LPS, lung tissues were collected for QRT-PCR analysis. n = 4. *, P < 0.01. (B) Pulmonary transvascular EBA flux demonstrating decreased lung vascular permeability of Pik3cg−/− mice transduced with FOXM1 plasmid DNA. At 60h post-LPS challenge, lungs were collected for EBA assay. n = 4. *, P < 0.01. (C) Normalized resolution of lung inflammation in Pik3cg−/− mice transduced with FOXM1 plasmid DNA. n = 4. *, P < 0.001. All statistical analyses were performed with t test.