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.

中文翻译：

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MiR-216a通过调节JAK2 / STAT3和NF-κB信号传导减轻LPS诱导的急性肺损伤。

MicroRNA（miRNA）在急性肺损伤（ALI）和急性呼吸窘迫综合征（ARDS）的进展中起重要作用。到目前为止，人们对miR-216a在ALI / ARDS中的作用了解甚少。在这项研究中，ARDS患者的白细胞介素-1β（IL-1β），白细胞介素6（IL-6）和肿瘤坏死因子-α（TNF-α）的水平显着高于健康对照组（P  <0.01）。但是，ARDS患者中miR-216a的表达明显低于健康对照组（P <0.05），并且与28天生存率呈负相关。在LPS处理的小鼠和A549细胞中观察到了相似的效果。MiR-216a过表达降低LPS诱导的IL-1β，IL-6和TNF-α水平，并改善肺通透性，并延长ALI小鼠的总生存期。此外，miR-216a过表达抑制LPS诱导的细胞凋亡和自噬。此外，janus激酶2（JAK2）是miR-216a的直接靶标。JAK2的沉默部分加剧了miR-216a抑制的炎症损伤。此外，miR-216a明显降低了磷酸化信号转导子和转录激活因子3（p-STAT3），p-p56和p-IκBα的表达。总之，miR-216a通过调节JAK2 / STAT3和NF-κB信号传导减轻LPS诱导的炎症损伤。