慢性阻塞性肺病
发病机制
巨噬细胞极化
细胞外小泡
上皮-间质转换
免疫学
医学
间充质干细胞
胞外囊泡
癌症研究
巨噬细胞
化学
细胞生物学
病理
生物
下调和上调
微泡
小RNA
内科学
体外
生物化学
基因
作者
Sheng Yang He,Duanni Chen,Mengyun Hu,Li Zhang,Caihong Liu,Daniela Traini,Georges E. Grau,Zhengpeng Zeng,Junjuan Lu,Guanzhi Zhou,Li Xie,Shenghua Sun
标识
DOI:10.1016/j.nano.2019.03.010
摘要
Chronic obstructive pulmonary disease (COPD) is partly characterized as epithelial–mesenchymal transition (EMT)-related airflow limitation. Extracellular vesicles (EVs) play crucial roles in the crosstalk between cells, affecting many diseases including COPD. Up to now, the roles of EVs in COPD are still debated. As we found in this investigation, COPD patients have higher miR-21 level in total serum EVs. EMT occurs in lungs of COPD mice. Furthermore, bronchial epithelial cells (BEAS-2B) could generate EVs with less miR-21 when treated with cigarette smoke extract (CSE), impacting less on the M2-directed macrophage polarization than the control-EVs (PBS-treated) according to EVs miR-21 level. Furthermore, the EMT processes in BEAS-2B cells were enhanced with the M2 macrophages proportion when co-cultured. Collectively, these results demonstrate that CSE-treated BEAS-2B cells could alleviate M2 macrophages polarization by modulated EVs, and eventually relieve the EMT process of BEAS-2B cells themselves under COPD pathogenesis, revealing a novel compensatory role of them in COPD.
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