FOXF1 maintains endothelial barrier function and prevents edema after lung injury

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Science Signaling  19 Apr 2016:
Vol. 9, Issue 424, pp. ra40
DOI: 10.1126/scisignal.aad1899

Improving endothelial barrier in the lung

Acute lung injury decreases the ability of the endothelial cells lining pulmonary blood vessels to be an effective barrier, resulting in the accumulation of fluid in the lungs (a condition called pulmonary edema) and inflammation. Cai et al. found that, in adult lung endothelial cells, the transcription factor FOXF1 transcriptionally activated a gene encoding the receptor for S1P, a lipid mediator that enhances the barrier function of endothelial cells. Adult mice that lacked one Foxf1 allele in lung endothelial cells were more likely to develop pulmonary edema and die after acute lung injury, outcomes that were reversed by administration of S1P. Thus, therapies that increase the activity of FOXF1 or S1P signaling could be used to decrease the complications that arise after acute lung injury, which can require hospitalization and can be fatal.

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