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 6
Failure of WT bone marrow cells to rescue the vascular repair defect in FoxM1 CKO mice following LPS challenge. (A) FACS analysis of GFP-positive bone marrow lymphocytes (lymph) and total white blood cells. At 3 weeks following transplantation of WT bone marrow cells isolated from GFP-transgenic mice, bone marrow cells were isolated from reconstituted FoxM1 CKO and red blood cells were lysed prior to FACS analysis. Bone marrow white blood cells isolated from C57B6 mice and GFP-transgenic mice were used as negative and positive controls, respectively. Approximately 80% of bone marrow reconstitution was achieved. BMT, WT bone marrow cell–transplanted FoxM1 CKO. (B) Sustained increase in lung microvessel permeability in WT bone marrow cell–transplanted FoxM1 CKO following LPS challenge. At 5 weeks following WT bone marrow transplantation, lungs from WT or FoxM1 CKO mice were isolated for K_f,c measurement. Data are expressed as mean ± SD, n = 3–5 per group. *P < 0.001 versus basal; **P < 0.001, CKO versus WT. Basal, 0.2 ml PBS. CKO, FoxM1 CKO mice reconstituted with WT bone marrow cells. (C) Quantitative analysis of FoxM1 mRNA expression in bone marrow cells. Bone marrow white blood cells were isolated from either WT or FoxM1 CKO at the indicated time points following LPS challenge, and RNA was isolated for QRT-PCR analysis. FoxM1 mRNA levels were normalized to cyclophilin. Data are expressed as mean ± SD, n = 3 per group. In contrast to endothelial cells isolated from FoxM1 CKO lungs, the white blood cells from FoxM1 CKO bone marrow expressed FoxM1 at the same level as WT.