PM2.5 induces autophagy-mediated cell death via NOS2 signaling in human bronchial epithelium cells

Zhu, Xiaoming; Wang, Qin; Xing, Weiwei; Long, Minhui; Fu, Wenliang; Xia, Wenrong; Jin, Chen; Guo, Na; Xu, Dongqun; D, Xu

doi:10.7150/ijbs.24546

Cited by 77 publications

(46 citation statements)

References 34 publications

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“…A previous study indicated that PM2.5 activated a number of apoptosis pathways in human epithelial lung cells (L132) in culture (9). PM2.5 also induced autophagy-mediated cell death via NOS2 signaling in human bronchial epithelium cells (33). The direct toxic effect of PM2.5 on human umbilical vein endothelial cells provides a novel insight into the mechanism of cardiovascular diseases caused by PM2.5 exposure (34).…”

Section: Discussionmentioning

confidence: 95%

PM2.5 induces autophagy‑mediated cell apoptosis via PI3K/AKT/mTOR signaling pathway in mice bronchial epithelium cells

Han

Zhuang

2020

Exp Ther Med

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Air pollution can highly impact the respiratory system in healthy individuals. Studies have indicated that particles with an aerodynamic diameter of ≤2.5 µm (PM2.5) can be considered to be harmful for lung alveoli and bronchial epithelium cells. PM2.5 can be directly inhaled and can deeply penetrate into the lung alveoli, causing lung dysfunction. However, the toxicological mechanism mediated by PM2.5 for respiratory disease has still not been clearly determined. The purpose of the current study was to investigate the effects of PM2.5 on mouse bronchial epithelium cells (MBECs) and explored the possible mechanism mediated by PM2.5 in MBECs. The results of the current study indicated that PM2.5 markedly decreased lung function, including total lung capacity, residual volume, vital capacity and airway resistance in experimental mice. The results demonstrated that PM2.5 markedly induced inflammatory responses, oxidative injury and MBEC apoptosis. PM2.5 increased interleukin (IL)-1β and IL-6 expression, and reactive oxygen species production in MBECs. Furthermore, PM2.5 specifically induced PI3K, AKT and mTOR expression in MBECs. Disruption of PI3K/AKT/mTOR signaling was also indicated to effectively inhibit apoptosis of MBECs. In conclusion, the results of the current study systematically demonstrated the role of apoptosis-mediated MBEC apoptosis in PM2.5-treated mice, and provides a potential strategy for preclinical intervention in patients with PM2.5-induced lung diseases.

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Section: Discussionmentioning

confidence: 95%

PM2.5 induces autophagy‑mediated cell apoptosis via PI3K/AKT/mTOR signaling pathway in mice bronchial epithelium cells

Han

Zhuang

2020

Exp Ther Med

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“…It has been widely reported that exposure to PM2.5 for a long time can be consistently correlated with a high mortality rate due to the components of PM2.5 consisting of nitrogen dioxide (NO 2 ) and SiO 2 . PM2.5 induces the expression of nitric oxide synthase 2 (NOS2) and subsequently generates NO, which elevates excessive autophagic effects . Furthermore, PM2.5 could accelerate the apoptotic response of airway epithelial cells in the pathogenesis of COPD .…”

Section: Discussionmentioning

confidence: 99%

Melatonin enhances autophagy and decreases apoptosis induced by nanosilica in RAW264.7 cells

Zhang

et al. 2019

IUBMB Life

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Melatonin is one of the main hormones that regulate biological rhythms and have immunomodulation, anti‐inflammatory, and antioxidation functions. In this study, we aimed to explore the effect of melatonin on the autophagy, apoptosis, and inflammatory reaction of macrophages (RAW264.7 cells) stimulated by nanosilica. SiO2 (100 mg/mL, 10–20 nm) was used to stimulate RAW264.7 cells at different time points (0, 2, 4, 8, 12, and 24 hr). Melatonin (200 μM) was added to SiO2‐stimulated macrophages at 12 hr. Beclin‐1, LC3, Bax, Bcl‐2, and Caspase‐3 were examined with western blotting. Flow cytometry was used to detect apoptosis. The levels of TNF‐α, IL‐1β, and IL‐18 were detected by ELISA. The level of TNF‐α in the supernatant of SiO2‐stimulated cells gradually increased with time but decreased following melatonin administration. In contrast, the expression of IL‐1β and IL‐18 increased after melatonin treatment. LC3 and Bax signaling pathways were activated in SiO2‐stimulated RAW264.7 cells, showing elevated expression of LC3 and reduced expression of Bax in the melatonin‐treated cells. GFP‐LC3 puncta were significantly increased in SiO2‐stimulated RAW264.7 cells and decreased in melatonin‐treated cells. The apoptotic rate in SiO2‐stimulated RAW264.7 cells increased with time and decreased after melatonin treatment, and the number of phagosomes increased with the stimulation of nanosilica and the treatment of melatonin. Melatonin might promote autophagy and inhibit apoptosis as well as inflammatory responses of RAW264.7 cells stimulated by nanosilica. © 2019 IUBMB Life, 2019

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“…PM and O 3 exposure can regulate autophagy. 125,202,[210][211][212][213] Whether effects of pollutant exposure on autophagy alter coronavirus assembly and replication is unknown (Fig. 2).…”

Section: Pollutant Exposure Interferes With Mitochondrial Function Anmentioning

confidence: 99%

SARS‐CoV‐2 infection, COVID‐19 pathogenesis, and exposure to air pollution: What is the connection?

Woodby

Arnold

Valacchi

2020

Annals of the New York Academy of Sciences

131

113

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Exposure to air pollutants has been previously associated with respiratory viral infections, including influenza, measles, mumps, rhinovirus, and respiratory syncytial virus. Epidemiological studies have also suggested that air pollution exposure is associated with increased cases of SARS-CoV-2 infection and COVID-19-associated mortality, although the molecular mechanisms by which pollutant exposure affects viral infection and pathogenesis of COVID-19 remain unknown. In this review, we suggest potential molecular mechanisms that could account for this association. We have focused on the potential effect of exposure to nitrogen dioxide (NO 2), ozone (O 3), and particulate matter (PM) since there are studies investigating how exposure to these pollutants affects the life cycle of other viruses. We have concluded that pollutant exposure may affect different stages of the viral life cycle, including inhibition of mucociliary clearance, alteration of viral receptors and proteases required for entry, changes to antiviral interferon production and viral replication, changes in viral assembly mediated by autophagy, prevention of uptake by macrophages, and promotion of viral spread by increasing epithelial permeability. We believe that exposure to pollutants skews adaptive immune responses toward bacterial/allergic immune responses, as opposed to antiviral responses. Exposure to air pollutants could also predispose exposed populations toward developing COIVD-19associated immunopathology, enhancing virus-induced tissue inflammation and damage.

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PM2.5 induces autophagy-mediated cell death via NOS2 signaling in human bronchial epithelium cells

Cited by 77 publications

References 34 publications

PM2.5 induces autophagy‑mediated cell apoptosis via PI3K/AKT/mTOR signaling pathway in mice bronchial epithelium cells

PM2.5 induces autophagy‑mediated cell apoptosis via PI3K/AKT/mTOR signaling pathway in mice bronchial epithelium cells

Melatonin enhances autophagy and decreases apoptosis induced by nanosilica in RAW264.7 cells

SARS‐CoV‐2 infection, COVID‐19 pathogenesis, and exposure to air pollution: What is the connection?

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PM2.5 induces autophagy-mediated cell death via NOS2 signaling in human bronchial epithelium cells

Cited by 77 publications

References 34 publications

PM2.5&nbsp;induces autophagy‑mediated cell apoptosis via PI3K/AKT/mTOR signaling pathway in mice bronchial epithelium cells

PM2.5&nbsp;induces autophagy‑mediated cell apoptosis via PI3K/AKT/mTOR signaling pathway in mice bronchial epithelium cells

Melatonin enhances autophagy and decreases apoptosis induced by nanosilica in RAW264.7 cells

SARS‐CoV‐2 infection, COVID‐19 pathogenesis, and exposure to air pollution: What is the connection?

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PM2.5 induces autophagy‑mediated cell apoptosis via PI3K/AKT/mTOR signaling pathway in mice bronchial epithelium cells

PM2.5 induces autophagy‑mediated cell apoptosis via PI3K/AKT/mTOR signaling pathway in mice bronchial epithelium cells