Attenuation of PM2.5-Induced Lung Injury by 4-Phenylbutyric Acid: Maintenance of [Ca2+]i Stability between Endoplasmic Reticulum and Mitochondria

被引:0
|
作者
Ma, Zhenhua [1 ,2 ]
Du, Xiaohui [1 ]
Sun, Yize [1 ]
Jia, Yunna [1 ]
Liang, Xiaojun [2 ]
Gao, Yunhang [1 ]
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; ER STRESS; PM2.5; EXPOSURE; INFLAMMATION;
D O I
10.3390/biom14091135
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
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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页数:18
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