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

PURPOSE

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 () in BPD .

MATERIALS AND METHODS

Blood samples from BPD patients and healthy volunteers were gathered, and an model of BPD was developed in alveolar epithelial cells (AECs) MLE-12 induced by hyperoxia. Then expression of krüppel-like factor 4 (/) and / were evaluated. After 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 and promoter predicted on the JASPAR website was verified using luciferase and ChIP assays. For further study of the mechanism of and in BPD, gain-of-function experiments were performed.

RESULTS

The mRNA levels of / and / were diminished in clinical BPD serum samples and hyperoxia-induced MLE-12 cells. Overexpression of stimulated AEC proliferation and suppressed AEC apoptosis induced by hyperoxia. Mechanically, bound to 's promoter region and aids transcription. Moreover, the results of gain-of-function experiments supported that could impede AEC damage induced by hyperoxia via stimulating .

CONCLUSION

and expression levels were declined in hyperoxia-induced AECs, and could be transcriptionally activated by and protect against hyperoxia-induced AEC injury in BPD. As a result, might become a prospective therapeutic target for BPD.