Attenuation of PM2.5-Induced Lung Injury by 4-Phenylbutyric Acid: Maintenance of [Ca2+]i Stability between Endoplasmic Reticulum and Mitochondria
文献类型： 外文期刊
作者： Ma, Zhenhua 1 ; Du, Xiaohui 1 ; Sun, Yize 1 ; Jia, Yunna 1 ; Liang, Xiaojun 2 ; Gao, Yunhang 1 ;
作者机构： 1.Jilin Agr Univ, Coll Anim Sci & Technol, Changchun 130118, Peoples R China
2.Ningxia Acad Agr & Forestry Sci, Inst Anim Sci, Yinchuan 750002, Peoples R China
关键词： PM2.5; 4-PBA; intracellular Ca2+; ER stress; mitochondrial damage; pyroptosis
期刊名称：BIOMOLECULES （ 影响因子：4.8； 五年影响因子：5.6 ）
ISSN：
年卷期： 2024 年 14 卷 9 期
页码：
收录情况： SCI
摘要： Fine particulate matter (PM2.5) is a significant cause of respiratory diseases and associated cellular damage. The mechanisms behind this damage have not been fully explained. This study investigated two types of cellular damage (inflammation and pyroptosis) induced by PM2.5, focusing on their relationship with two organelles (the endoplasmic reticulum and mitochondria). Animal models have demonstrated that PM2.5 induces excessive endoplasmic reticulum stress (ER stress), which is a significant cause of lung damage in rats. This was confirmed by pretreatment with an ER stress inhibitor (4-Phenylbutyric acid, 4-PBA). We found that, in vitro, the intracellular Ca2+ ([Ca2+]i) dysregulation induced by PM2.5 in rat alveolar macrophages was associated with ER stress. Changes in mitochondria-associated membranes (MAMs) result in abnormal mitochondrial function. This further induced the massive expression of NLRP3 and GSDMD-N, which was detrimental to cell survival. In conclusion, our findings provide valuable insights into the relationship between [Ca2+]i dysregulation, mitochondrial damage, inflammation and pyroptosis under PM2.5-induced ER stress conditions. Their interactions ultimately have an impact on respiratory health.
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