Endothelial cell–restricted disruption of FoxM1 impairs endothelial repair following LPS-induced vascular injury
J. Clin. Invest. You-Yang Zhao, et al. 116:2333 doi:10.1172/JCI27154 [Go to this article.]

Figure 4
FoxM1 CKO mice exhibit endothelial apoptosis and lung neutrophil sequestration similar to that of WT mice in the early period following LPS challenge. (A) Representative micrographs of TUNEL staining. Cryosections of lungs (3- to 5-μm thick) collected 24 hours after LPS challenge were stained with FITC-conjugated TUNEL to identify apoptotic cells and anti-vWF antibody to identify endothelial cells; nuclei were counterstained with DAPI. Arrows, TUNEL⁺vWF⁺ cells. Scale bar: 25 mm. (B) Graphic representation of apoptotic endothelial cells and nonendothelial cells in FoxM1 CKO and WT lungs 24 hours after LPS challenge (5 mg/kg BW). The number of TUNEL-positive nuclei and vWF-positive cells from 3 to 4 consecutive cryosections from each mouse lung were averaged. Data are expressed as mean ± SD, n = 3–4 mice per group. There is no difference between WT and FoxM1 CKO. (C) Lung tissue myeloperoxidase (MPO) activity during basal period and 6 hours after LPS challenge (5 mg/kg BW). Data are expressed as mean ± SD, n = 4 mice per group. *P > 0.1 versus WT. Although there is a significant increase in MPO activity in mouse lungs 6 hours following LPS challenge, both WT and FoxM1 CKO lungs exhibit similar MPO activities, indicating a similar extent of polymorphonuclear leukocyte sequestration.