Long non-coding RNA MALAT1 plays a protective role in bronchopulmonary dysplasia via the inhibition of apoptosis and interaction with the Keap1/Nrf2 signal pathway.

Abstract

BackgroundBronchopulmonary dysplasia (BPD) is a common respiratory disease in premature infants and is characterized by alveolar and pulmonary vascular dysplasia. Long-term oxygen exposure can cause BPD in preterm infants. Numerous studies have shown that long non-coding ribonucleic acid (lncRNA) is involved in the process of biological metabolism; however, its role in the development of BPD is unclear. Apoptosis-induced factor (AIF) is a key component involved in apoptosis. The Kelch-like ECH-associated protein 1/nuclear factor erythroid-2-related factor 2 (Keap1/Nrf2) signaling pathway is a body-derived antioxidant signaling pathway.MethodsIn this study, the relative expression of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), AIF, Keap1, and Nrf2 was detected by real-time polymerase chain reaction (PCR). Also, the apoptosis of A549 cells was detected by flow cytometry.ResultsThe results showed that, compared to the control group, the expression of MALAT1 increased significantly, and AIF decreased substantially in BPD premature infants. In the A549 hyperoxic lung injury model, compared with the air group, the expression of MALAT1 in the hyperoxia group decreased markedly, while the expression of Keap1 and Nrf2 increased considerably. Furthermore, compared with the control plasmid transfection air group (NC group), the expression of Keap1 and Nrf2 increased significantly in the small interfering RNA (siRNA) group.ConclusionsThese results indicate that MALAT1 can play a protective role in BPD via the reduction of apoptosis and anti-oxidation, offering clinicians a new way to prevent and treat BPD.