Biomass-related PM2.5 induces mitochondrial fragmentation and dysfunction in human airway epithelial cells. (1st January 2022)

• Record Type: Journal Article
• Authors: Gao, Mi; Liang, Chunxiao; Hong, Wei; Yu, Xiaoyuan; Zhou, Yumin; Sun, Ruiting; Li, Haiqing; Huang, Haichao; Gan, Xuhong; Yuan, Ze; Zhang, Jiahuan; Chen, Juan; Mo, Qiudi; Wang, Luyao; Lin, Biting; Li, Bing; Ran, Pixin
• Is Part Of: Environmental pollution. Volume 292:Part B(2022)
• Publication Date: 2022-01-01
• Subjects: Biomass-related PM2.5 -- Chronic obstructive pulmonary disease (COPD) -- Mitochondria dysfunction; Pollution -- Periodicals; Pollution -- Environmental aspects -- Periodicals; Environmental Pollution -- Periodicals; Pollution -- Périodiques; Pollution -- Aspect de l'environnement -- Périodiques; Pollution -- Effets physiologiques -- Périodiques; Pollution; Pollution -- Environmental aspects; Periodicals; Electronic journals; 363.73
• DOI: 10.1016/j.envpol.2021.118464
• Languages: English
• ISSNs: 0269-7491

Abstract

Abstract: The use of biomass for cooking and heating is considered an important factor associated with chronic obstructive pulmonary disease (COPD), but few studies have previously addressed its underlying mechanisms. Therefore, this research aimed to evaluate the effects of biomass-related PM2.5 (BRPM2.5 ) exposure on 16HBE human airway epithelial cells and in mice with regard to mitochondrial dysfunction. Our study indicated that BRPM2.5 exposure of 16HBE cells resulted in mitochondrial dysfunction, including decreased mitochondrial membrane potential, increased expression of fission proteins-phospho-DRP1, increased mitochondrial ROS (mtROS), and decreased levels of ATP. BRPM2.5 altered the mitochondrial metabolism of 16HBE cells by decreasing mitochondrial oxygen consumption and glycolysis. However, Mitochondria targeted peptide SS-31 eliminated mitochondrial ROS and alleviated the ATP deficiency and proinflammatory cytokines release. BRPM2.5 exposure resulted in abnormal mitochondrial morphological alterations both in 16HBE and in lung tissue. Taken together, these results suggest that BRPM2.5 has detrimental effects on human airway epithelial cells, leading to mitochondrial dysfunction, abnormal mitochondrial metabolism and altered mitochondrial dynamics. The present study provides the first evidence that disruption of mitochondrial structure and mitochondrial metabolism may be one of the mechanisms of BRPM2.5 -induced respiratory dysfunction. Abstract : Biomass-related particulate (matter (<2.5 μm; PM2.5) (BRPM2.5) induced cellular reactive oxygen species (ROS) and mitochondrial ROS (mtROS) generation in 16HBE cells in does and time independent manner. BRPM2.5 reduced the ΔΨm (mitochondrial membrane potential), ATP level, mitochondrial human airway epithelial cells (OCR) and mitochondrial extracellular acidification rate (ECAR) in 16HBE cells (human airway epithelial cells). BRPM2.5 promoted mitochondrial fission proteins phospho-DRP1 at 48h. BRPM2.5 changed mitochondrial morphology in a COPD (chronic obstructive pulmonary disease) mouse model.