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 1
Mouse model of endothelial cell–restricted deletion of FoxM1. (A) Southern blot demonstrating recombination of the FoxM1 floxed allele in endothelial cell–enriched tissues. Mouse genomic DNA (15 μg /lane) was digested with Bgl II and XbaI. The blots were probed with 3′ probe as described (13). Tie2 promoter/enhancer-driven Cre expression created a predicted 7.6-kb band in the aorta and lungs. The pseudogene band is indicated by an asterisk. (13). fl, FoxM1 floxed allele; AA, aorta; L, lung. (B) Quantitative analysis of mRNA expression of FoxM1 and FoxO1 by QRT-PCR. RNA was extracted from lungs of either FoxM1 WT or FoxM1 CKO mice. mRNA expression of FoxM1 and FoxO1 was normalized to mouse cyclophilin mRNA. There were no differences in FoxM1 mRNA levels in mice with the 3 genotypes FoxM1^+/+, FoxM1^fl/+, and FoxM1^fl/fl; therefore, all these mice were referred to as WT mice. Data are expressed as mean ± SD, n = 3. **P < 0.05. CKO, FoxM1 CKO. (C) Quantitative analysis of FoxM1 expression in population of cells either enriched or depleted of endothelial cells. RNA was extracted from an endothelial cell–enriched primary culture (EC, passage 0) isolated from mouse lungs or from nonendothelial cell primary cultures (non-EC, passage 4), fibroblasts, and epithelial cells. Approximately 70% reduction of FoxM1 mRNA levels was detected in FoxM1 CKO EC and not in FoxM1 CKO non-EC (n = 3), indicating endothelial cell–specific knockdown of FoxM1. ^#P < 0.01. n = 3.