Oxidative stress activates the TRPM2-Ca2+-NLRP3 axis to promote PM2.5-induced lung injury of mice

Wang, Chun-Yuan; Meng, Xianzong; Meng, Meiling; Shi, Min; Sun, Wenping; Li, Xiaojing; Zhang, Xiao; Liu, Ruihao; Fu, Ying; Song, Laiyu

doi:10.1016/j.biopha.2020.110481

Cited by 27 publications

(13 citation statements)

References 43 publications

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“…Previous studies have shown that PM 2.5 pollution produces premature death globally and is the largest environmental cause of diseases (Yang et al 2018). Results of a large population-based cohort study of approximately 1.1 million people over a period of 10 years showed a causal relationship demonstrating a positive association between PM 2.5 and lung injuries (Weichenthal et al 2017), as well as an increased risk of respiratory morbidity and mortality (Pun et al 2017;Wang et al 2020). The PM used in this study was < 2.5 μm in diameter, and able to penetrate into the alveolar regions of the lung to damage the AMs (Deng et al 2013;Draijer and Peters-Golden 2017).…”

Section: Discussionmentioning

confidence: 98%

Cytotoxicity induced by fine particulate matter (PM2.5) via mitochondria-mediated apoptosis pathway in rat alveolar macrophages

Wei

Yuan

et al. 2021

Environ Sci Pollut Res

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Although positive associations exist between ambient particulate matter (PM 2.5 ; diameter ≤ 2.5 μm) and the morbidity and mortality rates for respiratory diseases, the biological mechanisms of the reported health effects are unclear. Considering that alveolar macrophages (AM) are the main cells responsible for phagocytic clearance of xenobiotic particles that reach the airspaces of the lungs, the purpose of this study was to investigate whether PM 2.5 induced AM apoptosis, and investigate its possible mechanisms. Freshly isolated AM from Wistar rats were treated with extracted PM 2.5 at concentrations of 33, 100, or 300 μg/mL for 4 h; thereafter, the cytotoxic effects were evaluated. The results demonstrated that PM 2.5 induced cytotoxicity by decreasing cell viability and increasing lactate dehydrogenase (LDH) levels in AMs. The levels of reactive oxygen species (ROS) and intracellular calcium cations (Ca 2+) markedly increased in higher PM 2.5 concentration groups. Additionally, the apoptotic ratio increased, and the apoptosis-related proteins BCL2-associated X (Bax), caspase-3, and caspase-9 were upregulated, whereas B cell lymphoma-2 (Bcl-2) protein levels were downregulated following PM 2.5 exposure. Cumulative findings showed that PM 2.5 induced apoptosis in AMs through a mitochondrial-mediated pathway, which indicated that PM 2.5 plays a significant role in lung injury diseases.

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Section: Discussionmentioning

confidence: 98%

Cytotoxicity induced by fine particulate matter (PM2.5) via mitochondria-mediated apoptosis pathway in rat alveolar macrophages

Wei

Yuan

et al. 2021

Environ Sci Pollut Res

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“…Exposure to PM 2.5 induce intracellular ATP decrease, which is linked with K + efflux, Ca 2+ influx, lysosome rupture, mitochondria disfunction, endoplasmic reticulum stress, and subsequently activate NLRP3 inflammasome pulmonary inflammation (Jia et al 2021). Furthermore, PM 2.5 induces intracellular ROS and subsequently lung injury such as lung inflammation and fibrosis, inhibition of blood vessel formation, and cornea inflammation by activating the NLRP3 inflammasome (Niu et al 2021;Shen et al 2019;Wang et al 2020a;Zheng et al 2018). In addition, exposure to PM 2.5 leads to cardiac dysfunction and injury, which are mediated by macrophage polarization and activation of the NLRP3 inflammasome in mice with apolipoprotein E -/- (Du et al 2019).…”

Section: Pm 25 Exposure and Nlrp3 Inflammasome Activationmentioning

confidence: 99%

“…Mitochondria as the center of biological energy of cells plays an important role in airborne particulate matter-induced immunotoxicity (Sharma et al 2021 ). Although several studies have suggested that there is an association between PM 2.5 exposure and NLRP3 inflammasome activation, the underlying mechanisms are still unknown (Cheng et al 2020 ; Duan et al 2019 ; Jia et al 2021 ; Niu et al 2021 ; Wang et al 2020a ). Furthermore, several reports showed that there is an association between PM 2.5 exposure and decreased intracellular ATP (Duan et al 2019 ; Jin et al 2019a ; Jin et al 2019b ; Ning et al 2019 ).…”

Section: Introductionmentioning

confidence: 99%

PM2.5 exposure inducing ATP alteration links with NLRP3 inflammasome activation

Zeng

Liu

et al. 2022

Environ Sci Pollut Res

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Fine particulate matter (PM 2.5 ) has been the primary air pollutant and the fourth leading risk factor for disease and death in the world. Exposure to PM 2.5 is related to activation of the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, but the mechanism of PM 2.5 affecting the NLRP3 inflammasome is still unclear. Previous studies have shown that PM 2.5 can cause alterations in adenosine triphosphate (ATP), and an increase in extracellular ATP and a decrease in intracellular ATP can trigger the activation process of the NLRP3 inflammasome. Therefore, we emphasize that ATP changes may be the central link and key mechanism of PM 2.5 exposure that activates the NLRP3 inflammasome. This review briefly elucidates and summarizes how PM 2.5 acts on ATP and subsequently further impacts the NLRP3 inflammasome. Investigation of ATP changes due to exposure to PM 2.5 may be essential to regulate NLRP3 inflammasome activation and treat inflammation-related diseases such as coronavirus disease 2019 (COVID-19). KeywordsPM 2.5 . ATP . Energy metabolism . NLRP3 inflammasome . COVID-19 Abbreviations PM 2.5 fine particulate matter NLRP3 NOD-like receptor family pyrin domain containing 3 ATP adenosine triphosphate COVID-19 coronavirus disease 2019 PAHs polycyclic aromatic hydrocarbons ASC apoptosis-associated speck-like protein K + potassium Ca 2+ calcium Na + sodium IL-1β interleukin-1β IL-18 interleukin-18 TCA tricarboxylic acid ROS reactive oxygen species NADPH nicotinamide adenine dinucleotide phosphate DNA deoxyribonucleic acid * Xiang Zeng

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“…Li et al 57 found that PM 2.5 can regulate the activation of NLRP3 inflammasome through the circBbs9‐miR‐30e5p‐Adar pathway (Figure 2). The study of Wang et al 58 also proved the positive role of ROS‐TRPM2‐Ca2 + ‐NLRP3 pathway in PM 2.5‐induced lung injury (Figure 2). The above experiments demonstrate that PM2.5 can activate the NLRP3 inflammasome through multiple pathways, providing a new targeted therapeutic idea for the treatment of PM2.5‐induced lung injury.…”

Section: Nlrp3 and Copdmentioning

confidence: 73%

The role of the NLRP3 inflammasome in chronic inflammation in asthma and chronic obstructive pulmonary disease

Zhao

et al. 2022

Immunity Inflam & Disease

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Asthma and chronic obstructive pulmonary disease (COPD) are lung diseases characterized by airflow limitation and chronic inflammation. More and more studies have shown that the occurrence and development of asthma and COPD are related to abnormal immune responses caused by dysregulation of many genetic and environmental factors. The exact pathogenesis of the disease is still unclear. A large number of studies have shown that the NLRP3 inflammasome is involved in the process of chronic airway inflammation in asthma and COPD. Here, we summarize recent advances in the mechanism of NLRP3 inflammasome activation and regulation and its role in the pathogenesis of inflammatory lung diseases such as asthma and COPD. Meanwhile we propose possible therapeutic targets in asthma and COPD.

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Oxidative stress activates the TRPM2-Ca2+-NLRP3 axis to promote PM2.5-induced lung injury of mice

Cited by 27 publications

References 43 publications

Cytotoxicity induced by fine particulate matter (PM2.5) via mitochondria-mediated apoptosis pathway in rat alveolar macrophages

Cytotoxicity induced by fine particulate matter (PM2.5) via mitochondria-mediated apoptosis pathway in rat alveolar macrophages

PM2.5 exposure inducing ATP alteration links with NLRP3 inflammasome activation

The role of the NLRP3 inflammasome in chronic inflammation in asthma and chronic obstructive pulmonary disease

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