Atmospheric fine particulate matter (PM2.5) induces pulmonary fibrosis by regulating different cell fates via autophagy

被引:3
|
作者
Liu, Bingyan [1 ]
Han, Yangchen [1 ]
Ye, Yiyuan [1 ]
Wei, Xiaoran [2 ]
Li, Gang [3 ]
Jiang, Wei [1 ]
机构
[1] Shandong Univ, Environm Res Inst, Qingdao 266237, Peoples R China
[2] Qingdao Univ, Sch Publ Hlth, Dept Occupat & Environm Hlth, Qingdao 266071, Peoples R China
[3] Chinese Acad Sci, Res Ctr Ecoenvironm Sci, State Key Lab Environm Chem & Ecotoxicol, Beijing 100085, Peoples R China
基金
中国国家自然科学基金;
关键词
PM2.5; Pulmonary fibrosis; Autophagy; Mitophagy; Parkin; CHEMICAL-COMPOSITION; QUALITY-CONTROL; GLOBAL BURDEN; PATHOGENESIS; PROMOTES; DISEASE; HOMEOSTASIS; PREVALENCE; MECHANISMS; MITOPHAGY;
D O I
10.1016/j.scitotenv.2024.171396
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
The presence of respiratory diseases demonstrates a positive correlation with atmospheric fine particulate matter (PM2.5) exposure. The respiratory system is the main target organ affected by PM2.5, and exposure to PM2.5 elevates the likelihood of developing pulmonary fibrosis (PF). In this study, lung epithelial cell (BEAS-2B) and fibroblast (NIH-3T3) were used as in vitro exposure models to explore the mechanisms of PF. PM2.5 exposure caused mitochondrial damage in BEAS-2B cells and increased a fibrotic phenotype in NIH-3T3 cells. Epithelial cells and fibroblasts have different fates after PM2.5 exposure due to their different sensitivities to trigger autophagy. Exposure to PM2.5 inhibits mitophagy in BEAS-2B cells, which hinders the removal of damaged mitochondria and triggers cell death. In this process, the nuclear retention of the mitophagy-related protein Parkin prevents it from being recruited to mitochondria, resulting in mitophagy inhibition. In contrast, fibroblasts exhibit increased levels of autophagy, which may isolate PM2.5 and cause abnormal fibroblast proliferation and migration. Fibrotic phenotypes such as collagen deposition and increased alpha-actin also appear in fibroblasts. Our results identify PM2.5 as a trigger of PF and delineate the molecular mechanism of autophagy in PM2.5 induced PF, which provides new insights into the pulmonary injury.
引用
收藏
页数:14
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