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Bronchopulmonary dysplasia (BPD) is a long-term respiratory condition. More than a quarter of extremely premature newborns are harmed by BPD. At present, there are no apparent effective drugs or treatments for the condition. In this study, we aimed to investigate the functional role and mechanism of lymphoid enhancer-binding factor 1 ( Lef1 ) in BPD  in vitro . Blood samples from BPD patients and healthy volunteers were gathered, and an  in vitro  model of BPD was developed in alveolar epithelial cells (AECs) MLE-12 induced by hyperoxia. Then expression of krüppel-like factor 4 ( KLF4 / Klf4 ) and  LEF1 / Lef1  were evaluated. After  Lef1  overexpressing plasmid and the vector were transfected into hyperoxia-induced MLE-12 cells, cell proliferation assays were carried out. Cell apoptosis was investigated by a flow cytometry assay, and apoptosis related proteins Bcl-2, cleaved-caspase 3 and 9 were analyzed by a western blot assay. The binding between  Klf4  and  Lef1  promoter predicted on the JASPAR website was verified using luciferase and ChIP assays. For further study of the mechanism of  Klf4  and  Lef1  in BPD, gain-of-function experiments were performed. The mRNA levels of  KLF4 / Klf4  and  LEF1 / Lef1  were diminished in clinical BPD serum samples and hyperoxia-induced MLE-12 cells. Overexpression of  Lef1  stimulated AEC proliferation and suppressed AEC apoptosis induced by hyperoxia. Mechanically,  Klf4  bound to  Lef1 ’s promoter region and aids transcription. Moreover, the results of gain-of-function experiments supported that  Klf4  could impede AEC damage induced by hyperoxia via stimulating  Lef1 . Klf4  and  Lef1  expression levels were declined in hyperoxia-induced AECs, and  Lef1  could be transcriptionally activated by  Klf4  and protect against hyperoxia-induced AEC injury in BPD. As a result,  Lef1  might become a prospective therapeutic target for BPD.

Lef1 is transcriptionally activated by Klf4 and suppresses hyperoxia-induced alveolar epithelial cell injury