Lung epithelial-mesenchymal transition (EMT) plays an important role in silicosis fibrosis. The reverse process of EMT is mesenchymal-epithelial transition (MET), which is viewed as an anti-EMT therapy and is a good target toward fibrosis. MicroRNAs (miRNAs) have emerged as potent regulators of EMT and MET programs, and, hence, we tested the miRNA expression using microarray assay and investigated their roles in silica-induced EMT in lung epithelial cells. We found that miRNA-29b (miR-29b) was dynamically downregulated by silica and influenced the promotion of MET in RLE-6TN cells. Furthermore, delivery of miR-29b to mice significantly inhibited silica-induced EMT, prevented lung fibrosis, and improved lung function. Together, our results clearly demonstrated that miR-29b acted as a novel negative regulator of silicosis fibrosis-inhibited lung fibrosis, probably by promoting MET and by suppressing EMT in the lung. These findings may represent a new potential therapeutic target for treating silicosis fibrosis.

肺上皮-间质转化（EMT）在矽肺纤维化中起重要作用。EMT的逆过程是间充质-上皮转化（MET），它被视为一种抗EMT治疗，并且是纤维化的良好靶标。MicroRNA（miRNA）已成为EMT和MET程序的有效调节剂，因此，我们使用微阵列分析法测试了miRNA的表达，并研究了它们在二氧化硅诱导的肺上皮细胞EMT中的作用。我们发现，miRNA-29b（miR-29b）被二氧化硅动态下调，并影响了RLE-6TN细胞中MET的促进作用。此外，将miR-29b递送至小鼠可显着抑制二氧化硅诱导的EMT，预防肺纤维化并改善肺功能。一起，我们的结果清楚地表明，miR-29b可能是通过促进MET并抑制肺中的EMT来充当矽肺病纤维化抑制的肺纤维化的新型负调节剂。这些发现可能代表了治疗矽肺纤维化的新的潜在治疗靶标。