MiR-206 inhibits FN1 expression and proliferation and promotes apoptosis of rat type II alveolar epithelial cells.

Abstract

Bronchopulmonary dysplasia (BPD) is a syndrome of respiratory distress caused by chronic lung injury, primarily in preterm infants. miR-206 and fibronectin 1 (FN1) are associated with the development of BPD. The present study used rat type II alveolar epithelial cells (AECII) to investigate the underlying mechanisms of BPD. AECII were isolated using a primary cell culture prior to alkaline phosphatase staining and immunofluorescence of surfactant protein C (SP-C). These were used to verify the presence of AECII. AECII were then divided into four groups, which were transfected with four different plasmids. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to determine the relative expression of miR-206 in the each group. The gene and protein expression level of FN1 was detected by RT-qPCR and immunofluorescence. The proliferation of AECII in each of the four groups was evaluated using an MTT assay 48 h following transfection. The percentage of apoptotic cells was determined by flow cytometric analysis. The present study demonstrated that upregulation of miR-206 decreased the expression of FN1 (P<0.05) and low levels of miR-206 led to increased expression of FN1 (P<0.05) in AECII. Furthermore, the forced expression of miR-206 suppressed proliferation and promoted apoptosis of AECII while downregulation of miR-206 had the opposite effect (P<0.05). The results of the current study provide valuable insights into the prevention of BPD and suggest that miR-206 may be used as a potential molecular target for BPD therapy in the future.