MiR-216a alleviates LPS-induced acute lung injury via regulating JAK2/STAT3 and NF-κB signaling.

MicroRNAs (miRNAs) play an important role in the progression of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Till now, little is known about the role of miR-216a in ALI/ARDS. In this study, patients with ARDS exhibited significantly higher interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) levels than healthy controls (P < 0.01). However, miR-216a expression in patients with ARDS was significantly lower than healthy controls (P < 0.05), and negatively correlated with 28-day survival rate. Similar effects were observed in LPS-treated mice and A549 cells. MiR-216a over-expression reduced LPS-induced IL-1β, IL-6 and TNF-α levels, and ameliorated lung permeability, and prolonged overall survival of ALI mice. Further, miR-216a over-expression inhibited LPS-induced apoptosis and autophagy. In addition, the janus kinase-2 (JAK2) was a direct target of miR-216a. Silencing of JAK2 partially aggravated miR-216a-inhibited inflammation injury. Besides, miR-216a obviously decreased the expressions of phosphorylated signal transducer and the activator of transcription 3 (p-STAT3), p-p56, and p-IκBα. In conclusion, miR-216a alleviates LPS-induced inflammatory injury via regulating JAK2/STAT3 and NF-κB signaling.