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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 1.

Figure 1

p110γ mediates FoxM1 expression during the repair phase following LPS challenge. (A) FoxM1 mRNA expression in lungs. At 12h post-LPS, WT mice were administered either DMSO (CTL) or wortmannin (Wor, 0.05mg/kg BW, i.p.) every 12 h. Lung tissue was collected for QRT-PCR analysis. n = 5 mice/group. *, P < 0.05; **, P < 0.01 (Student t test). (B) Representative Western blotting demonstrating decreased FoxM1 protein expression induced by wortmannin treatment. The experiment was repeated twice with similar results. (C) Inhibition of p110γ but not p110α decreased FoxM1 expression. At 12 h post-LPS, WT mice were administered either DMSO (CTL), the p110γ inhibitor AS-605240 (AS) (30 mg/kg, per os.), or the p110α inhibitor PI-103 (10 mg/kg, i.p.) at 12 h intervals. Lungs at 72h post-LPS were collected for QRT-PCR analysis. n = 5. *, P < 0.05 (ANOVA). (D) Inhibition of FoxM1 expression in Pik3cg−/− mouse lungs following LPS challenge. n = 5. *, P < 0.05; **, P < 0.01 (Student’s t test).