PM2.5 deregulated microRNA and inflammatory microenvironment in lung injury

Liu, Guangyan; Li, Yunxia; Zhou, Jiaming; Xu, Jia; Yang, Biao

doi:10.1016/j.etap.2022.103832

Cited by 23 publications

(8 citation statements)

References 48 publications

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“…In our studies, PM2.5 exposure enhanced invasion and migration capabilities, altered gene expression associated with ROS pathways, increased ROS production and disrupted mitochondrial membrane potential. This agrees with the recent studies; PM2.5 can cause oxidative stress 38 , 39 , cytotoxicity 40 , 41 , and affect the up or down-regulation of the release of mediators of the signaling pathway involved 41 , 42 . These findings significantly contribute to understanding of how PM2.5 impacts cellular function and health and have implications for environmental health research and potential intervention strategies.…”

Section: Discussionsupporting

confidence: 93%

Evaluation of Pm2.5 Influence on Human Lung Cancer Cells Using a Microfluidic Platform

Nguyen,

Hsieh,

Chin

et al. 2024

Int. J. Med. Sci.

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In this study, we developed a microfluidic device that is able to monitor cell biology under continuous PM2.5 treatment. The effects of PM2.5 on human alveolar basal epithelial cells, A549 cells, and uncovered several significant findings were investigated. The results showed that PM2.5 exposure did not lead to a notable decrease in cell viability, indicating that PM2.5 did not cause cellular injury or death. However, the study found that PM2.5 exposure increased the invasion and migration abilities of A549 cells, suggesting that PM2.5 might promote cell invasiveness. Results of RNA sequencing revealed 423 genes that displayed significant differential expression in response to PM2.5 exposure, with a particular focus on pathways associated with the generation of reactive oxygen species (ROS) and mitochondrial dysfunction. Real-time detection demonstrated an increase in ROS production in A549 cells after exposure to PM2.5. JC1 assay, which indicated a loss of mitochondrial membrane potential (ΔΨm) in A549 cells exposed to PM2.5. The disruption of mitochondrial membrane potential further supports the detrimental effects of PM2.5 on A549 cells. These findings highlight several adverse effects of PM2.5 on A549 cells, including enhanced invasion and migration capabilities, altered gene expression related to ROS pathways, increased ROS production and disruption of mitochondrial membrane potential. These findings contribute to our understanding of the potential mechanisms through which PM2.5 can impact cellular function and health.

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Section: Discussionsupporting

confidence: 93%

Evaluation of Pm2.5 Influence on Human Lung Cancer Cells Using a Microfluidic Platform

Nguyen,

Hsieh,

Chin

et al. 2024

Int. J. Med. Sci.

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“…Acute lung injury is mostly caused by PM2.5, cellular characteristics include loss of alveolar-capillary membrane integrity, transepithelial migration of AGING neutrophils and macrophages, and increases in proinflammatory/cytotoxic proteins, Persistent exposure of PM2.5 result in pulmonary destruction, fibrosing alveolitis and lung organism failure [7]. The immune system, especially the macrophages, represent as the susceptible and powerful defense mechanism against the harmful factors, PM2.5 included [8,9], in normal conditions, alveolar macrophages will, through phagocytosis, immunity and secretion, immediately eliminate PM2.5, but when durative PM2.5 enter the respiratory system, the macrophages in lung become over-activated and bring about exacerbation of acute injury [10][11][12]. Activated macrophages secret proinflammatory cytokines (eg, TNFα, IFNs, interleukins), and generate cytotoxic reactive oxygen species (ROS) and proteolytic enzymes, and bioactive lipids, and moreover, extracellular traps (fibers composed of DNA and proteins) released from inflammatory macrophages in response to ROS, proteases, and TNFα in the pathogenic response to pulmonary toxicants deteriorate the acute lung injury [7,13].…”

Section: Introductionmentioning

confidence: 99%

MiR-217-5p inhibits smog (PM2.5)-induced inflammation and oxidative stress response of mouse lung tissues and macrophages through targeting STAT1

Xie

et al. 2022

Aging

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Objective: To explore the roles of macrophages’ miR-217-5p in the process of PM2.5 induced acute lung injury. Methods: GEO database and KEGG pathway enrichment analysis as well as GSEA were used to predicted the miRNA and associated target signals. And then mice and RAW246.7 macrophages treated with PM2.5 to imitate PM2.5 induced acute lung injury environment and then transfected with miR-217-5p NC or miR-217-5p mimic. The levels of inflammatory factors TNF-α and anti-inflammatory factor IL-10 of mice serum were tested by ELISA. And the pathological changes and ROS level of mouse lung tissues were stained by HE and DHE staining. The proteins expression of phosphorylated-STAT1, total-STAT1, TNF-α, IFN-γ as well as p47, gp91, NOX4 in mice or RAW264.7 cells were tested by western blot or immunofluorescence of RAW264.7 cell slides. Results: The results of bioinformatics analysis indicated the miR-217 as well as STAT1 were involved PM2.5 associated lung injury. After exposure to PM2.5, the decreased levels of serum TNF-α but not IL-10, consistent with reduced macrophages’ accumulation as well as decreased ROS levels in lung tissues in miR-217-5p mimic group vs miR-217-5p NC group mice, and moreover, the protein expression levels of phosphorylated--STAT1, total-STAT1, TNF-α, IFN-γ, p47, gp91 and NOX4 in mouse lung tissues and RTAW246.7 macrophages cells were all significantly reduced with miR-217-5p mimic administration. The above phenomena were reversed by specific STAT1-inhibitor HY-N8107. Conclusions: miR-217-5p suppressed the activated STAT1-signal induced inflammation and oxidative stress trigged by PM2.5 in macrophages and resulted in the decreased lung injure caused by PM2.5.

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“…It has attracted significant attention due to its adverse effects on climate, visibility, and especially human health [3][4][5][6]. Long-term exposure to PM 2.5 has been proven to increase the risk of lung cancer, dementia, cardiovascular disease, chronic respiratory diseases, and depressive-like responses [7][8][9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Characteristics of PM2.5 in an Industrial City of Northern China: Mass Concentrations, Chemical Composition, Source Apportionment, and Health Risk Assessment

Bai

Zhao

Yin

et al. 2022

IJERPH

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Urban and suburban PM2.5 samples were collected simultaneously during selected periods representing each season in 2019 in Zibo, China. Samples were analysed for water-soluble inorganic ions, carbon components, and elements. A chemical mass balance model and health risk assessment model were used to investigate the source contributions to PM2.5 and the human health risks posed by various pollution sources via the inhalation pathway. Almost 50% of the PM2.5 samples exceeded the secondary standard of China’s air quality concentration limit (75 µg/m3, 24 h). Water-soluble inorganic ions were the main component of PM2.5 in Zibo, accounting for 50 ± 8% and 56 ± 11% of PM2.5 at the urban and suburban sites, respectively. OC and OC/EC decreased significantly in the past few years due to enhanced energy restructuring. Pearson correlation analysis showed that traffic emissions were the main source of heavy metals. The Cr(VI) concentrations were 1.53 and 1.92 ng/m3 for urban and suburban sites, respectively, exceeding the national ambient air quality standards limit of 0.025 ng/m3. Secondary inorganic aerosols, traffic emissions, and secondary organic aerosols were the dominant contributors to PM2.5 in Zibo, with the total contributions from these three sources accounting for approximately 80% of PM2.5 and the remaining 20% attributed to traffic emissions. The non-carcinogenic risks from crustal dust for children were 2.23 and 1.15 in urban and suburban areas, respectively, exceeding the safe limit of 1.0 in both locations, as was the case for adults in urban areas. Meanwhile, the carcinogenic risks were all below the safe limit, with the non-carcinogenic and carcinogenic risks from traffic emissions being just below the limits. Strict control of precursor emissions, such as SO2, NOx, and VOCs, is a good way to reduce PM2.5 pollution resulting from secondary aerosols. Traffic control, limiting or preventing outdoor activities, and wearing masks during haze episodes may be also helpful in reducing PM2.5 pollution and its non-carcinogenic and carcinogenic health impacts in Zibo.

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PM2.5 deregulated microRNA and inflammatory microenvironment in lung injury

Cited by 23 publications

References 48 publications

Evaluation of Pm2.5 Influence on Human Lung Cancer Cells Using a Microfluidic Platform

Evaluation of Pm2.5 Influence on Human Lung Cancer Cells Using a Microfluidic Platform

MiR-217-5p inhibits smog (PM2.5)-induced inflammation and oxidative stress response of mouse lung tissues and macrophages through targeting STAT1

Characteristics of PM2.5 in an Industrial City of Northern China: Mass Concentrations, Chemical Composition, Source Apportionment, and Health Risk Assessment

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