Zeng Zhengpeng, He ShengYang, Lu JunJuan, Liu Chun, Lin Hua, Xu ChaoQun, Xie LiHua, Sun ShengHua
a Center for Experimental Medical Research , the Third Xiangya Hospital of Central South University , Changsha , Hunan , P.R. China.
b HuNan Cancer Hospital , Changsha , Hunan , P.R. China.
Exp Lung Res. 2018 Mar;44(2):89-97. doi: 10.1080/01902148.2018.1439548. Epub 2018 Mar 15.
MicroRNAs and autophagy play important roles in chronic obstructive pulmonary disease (COPD). This study was designed to explore the role of microRNA-21 (miR-21) induced autophagy in COPD. Using the C57BL/6, miR-21-/- mice and human bronchial epithelial (16HBE) cell line, we found that in the lung tissues of mice, the level of autophagy in the COPD model group was significantly higher than that in the control group. However, compared to the COPD model, the level of autophagy was significantly lower in the miR-21-/- CSE+CS group. In the COPD model, miR-21 was overexpressed. Moreover, in human bronchial epithelial (16HBE) cells exposed to cigarette smoke extract (CSE), miR-21 expression was upregulated and autophagy was notably increased. In addition, pretreatment of 16HBE cells with miR-21 inhibitor significantly inhibited autophagy activity and decreased apoptosis, indicating that miR-21 is involved in CSE-induced autophagy and apoptosis. The results showed that miR-21 could increase autophagy and promote the apoptosis of 16HBE cells in COPD. This information contributes to our further understanding of COPD.
微小RNA与自噬在慢性阻塞性肺疾病（COPD）中发挥着重要作用。本研究旨在探讨微小RNA-21（miR-21）诱导的自噬在COPD中的作用。利用C57BL/6、miR-21基因敲除小鼠及人支气管上皮（16HBE）细胞系，我们发现，在小鼠肺组织中，COPD模型组的自噬水平显著高于对照组。然而，与COPD模型相比，miR-21基因敲除的香烟烟雾提取物（CSE）+香烟烟雾组的自噬水平显著降低。在COPD模型中，miR-21呈过表达。此外，在暴露于香烟烟雾提取物（CSE）的人支气管上皮（16HBE）细胞中，miR-21表达上调且自噬显著增加。另外，用miR-21抑制剂预处理16HBE细胞可显著抑制自噬活性并减少细胞凋亡，表明miR-21参与了CSE诱导的自噬和细胞凋亡。结果显示，miR-21可增加COPD中16HBE细胞的自噬并促进其凋亡。这一信息有助于我们对COPD的进一步理解。
