MicroRNA-29b Mediates Lung Mesenchymal-Epithelial Transition and Prevents Lung Fibrosis in the Silicosis Model

作者：Sun, Jingping; Li, Qiuyue; Lian, Ximeng; Zhu, Zhonghui; Chen, Xiaowei; Pei, Wanying; Li, Siling; Abbas, Ali; Wang, Yan^*; Tian, Lin^*

来源：Molecular Therapy - Nucleic Acids, 2019, 14: 20-31.

DOI：10.1016/j.omtn.2018.10.017

• INDUCED PULMONARY-FIBROSIS
• REGULATOR
• MIR-29
• FAMILY

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.

• 出版日期2019-3-1
• 单位首都医科大学