自噬
PI3K/AKT/mTOR通路
慢性阻塞性肺病
免疫印迹
细胞生物学
程序性细胞死亡
化学
小干扰RNA
香烟烟雾
免疫学
癌症研究
医学
生物
细胞凋亡
信号转导
核糖核酸
毒理
内科学
生物化学
基因
作者
Lixing Wang,Furong Yan,Yongbin Shi,Xiaoshan Su,Yaping Zhang
标识
DOI:10.1016/j.tiv.2023.105711
摘要
The inhaling of cigarette smoke (CS) causes damage to airway epithelial cells, which is related to chronic obstructive pulmonary disease (COPD). It has been established that CS induces autophagy, but it is still unclear whether excessive or insufficient autophagy results in cell death. This study discovered that CS significantly elevates PSAT1 expression in bronchial epithelial cells. Further studies using autophagy inhibitor, RNA interference, RT-qPCR, western blot, and CCK-8 assay in 16-HBE cells have confirmed that autophagy is temporarily initiated by cigarette smoke extract (CSE), but insufficient autophagy leads to cell death. PSAT1 induced by CSE promotes autophagy and resists insufficient autophagy caused by CSE through Akt/mTOR pathway in human bronchial epithelial cells, playing a protective role.
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