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

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.