Clinical Center for Molecular Diagnosis and Therapy, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian, China.
Department of Pulmonary and Critical Care Medicine, The Second Affiliated Hospital of Fujian Medical University, Respirology Medicine Centre of Fujian Province, Quanzhou, Fujian, China.
Toxicol In Vitro. 2024 Feb;94:105711. doi: 10.1016/j.tiv.2023.105711. Epub 2023 Oct 12.
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.
吸烟会损害气道上皮细胞，这与慢性阻塞性肺疾病（COPD）有关。已经证实，吸烟会诱导自噬，但目前尚不清楚是过度自噬还是自噬不足会导致细胞死亡。本研究发现，吸烟会显著提高支气管上皮细胞中 PSAT1 的表达。进一步的研究使用自噬抑制剂、RNA 干扰、RT-qPCR、western blot 和 CCK-8 assay 在 16-HBE 细胞中证实，香烟烟雾提取物（CSE）会短暂引发自噬，但不足的自噬会导致细胞死亡。CSE 诱导的 PSAT1 通过 Akt/mTOR 通路促进自噬，抵抗 CSE 引起的不足的自噬，在人支气管上皮细胞中发挥保护作用。
