Recent advances in understanding the mechanisms of PM2.5-mediated neurodegenerative diseases

Zhu, Xiaoli; Ji, Xintong; Shou, Yikai; Huang, Yilu; Hu, Yu; Wang, Huanhuan

doi:10.1016/j.toxlet.2020.04.017

Cited by 34 publications

(20 citation statements)

References 90 publications

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“…In particular, lung and skin tissues have a structure that is vulnerable to fine dust due to direct damage from PM 2.5 , and damages in lung and skin tissues cause an inflammatory reaction by generating cytokines throughout the whole body [ 31 ]. In addition, PM 2.5 easily penetrates brain tissue and causes an inflammatory response of neuronal cells through the stimulation of microglial cells [ 32 ]. The systemic inflammatory response increases the production of free radicals, such as hydroxyl radicals and superoxide.…”

Section: Discussionmentioning

confidence: 99%

Powdered Green Tea (Matcha) Attenuates the Cognitive Dysfunction via the Regulation of Systemic Inflammation in Chronic PM2.5-Exposed BALB/c Mice

et al. 2021

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This study was conducted to evaluate the anti-amnesic effect of the aqueous extract of powdered green tea (matcha) (EM) in particulate matter (PM)2.5-induced systemic inflammation in BALB/c mice. EM ameliorated spatial learning and memory function, short-term memory function, and long-term learning and memory function in PM2.5-induced mice. EM protected against antioxidant deficit in pulmonary, dermal, and cerebral tissues. In addition, EM improved the cholinergic system through the regulation of acetylcholine (ACh) levels and acetylcholinesterase (AChE) activity in brain tissue, and it protected mitochondrial dysfunction by regulating the production of reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and ATP contents in brain tissue. EM attenuated systemic inflammation and apoptotic signaling in pulmonary, dermal, olfactory bulb, and hippocampal tissues. Moreover, EM suppressed neuronal cytotoxicity and cholinergic dysfunction in hippocampal tissue. This study suggests that EM might be a potential substance to improve PM2.5-induced cognitive dysfunction via the regulation of systemic inflammation.

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Section: Discussionmentioning

confidence: 99%

Powdered Green Tea (Matcha) Attenuates the Cognitive Dysfunction via the Regulation of Systemic Inflammation in Chronic PM2.5-Exposed BALB/c Mice

et al. 2021

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“…PM2.5 particles can interact with metals, inorganic particles, organic carbon, and microbes, resulting in toxic reactions, such as inflammation, DNA damage, reactive oxygen species (ROS) induction, and mitochondria dysfunction. These unusual responses in cells are related to the pathogenesis of a series of human diseases [ 28 , 29 , 30 ], such as emphysema in mice [ 31 ], lung cancer, and chronic airway inflammatory diseases [ 32 ]; the promotion of cancer stem cell properties [ 33 ]; the impairment sperm quality in mice [ 34 ]; the induction of allergic airway inflammation in mice [ 35 ]; and the development of Alzheimer’s disease [ 36 ], PM2.5 induces not only oxidative stress but also autophagy [ 37 , 38 ].…”

Section: Introductionmentioning

confidence: 99%

Micro- and Nanosized Substances Cause Different Autophagy-Related Responses

Wang

Zheng

Lee

et al. 2021

IJMS

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With rapid industrialization, humans produce an increasing number of products. The composition of these products is usually decomposed. However, some substances are not easily broken down and gradually become environmental pollutants. In addition, these substances may cause bioaccumulation, since the substances can be fragmented into micro- and nanoparticles. These particles or their interactions with other toxic matter circulate in humans via the food chain or air. Whether these micro- and nanoparticles interfere with extracellular vesicles (EVs) due to their similar sizes is unclear. Micro- and nanoparticles (MSs and NSs) induce several cell responses and are engulfed by cells depending on their size, for example, particulate matter with a diameter ≤2.5 μm (PM2.5). Autophagy is a mechanism by which pathogens are destroyed in cells. Some artificial materials are not easily decomposed in organisms. How do these cells or tissues respond? In addition, autophagy operates through two pathways (increasing cell death or cell survival) in tumorigenesis. Many MSs and NSs have been found that induce autophagy in various cells and tissues. As a result, this review focuses on how these particles interfere with cells and tissues. Here, we review MSs, NSs, and PM2.5, which result in different autophagy-related responses in various tissues or cells.

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“…These substances can pass through the nasal cavity, enter into the respiratory tract via the airflow and accumulate in tissues through diffusion or active transport ( Xing et al, 2016 ). previous studies have shown that PM 2.5 is associated with various respiratory disorders ( Xing et al, 2016 ), as well as cardiovascular ( Rajagopalan et al, 2018 ), neurodegenerative ( Zhu et al, 2020 ), and hepatic ( Tarantino et al, 2013 ) diseases. For instance, occurrence of nonalcoholic fatty liver disease – a known silent disease attacking about 20–30% of the population- was linked to exposure to PM 2.5 ( Sivell, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

CRISPR/Cas9-Mediated Whole Genomic Wide Knockout Screening Identifies Specific Genes Associated With PM2.5-Induced Mineral Absorption in Liver Toxicity

Peng

Wang

et al. 2021

Front. Bioeng. Biotechnol.

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PM2.5, also known as fine particles, refers to particulate matter with a dynamic diameter of ≦2.5 μm in air pollutants, that carries metals (Zn, Co, Cd) which can pass through the alveolar epithelium and enter the circulatory system and tissues. PM2.5 can cause serious health problems, such as non-alcoholic fatty liver and hepatocellular carcinoma, although the underlying mechanisms of its toxic effect are poorly understood. Here, we exposed L02 cells to PM2.5 and performed a pooled genome−wide clustered regularly interspaced short palindromic repeats/CRISPR-associated protein 9 (CRISPR/Cas9) to assess loss of function and identify new potential PM2.5targets. Enrichr and KEGG pathway analyses were performed to identify candidate genes associated with PM2.5 toxicity. Results revealed that four key genes, namely ATPase Na+/K+ transporting subunit alpha 2 (ATP1A2), metallothionein 1M (MT1M), solute carrier family 6 members 19 (SLC6A19) and transient receptor potential cation channel subfamily V member 6 (TRPV6) were associated with PM2.5 toxicity, mainly in regulating the mineral absorption pathway. Downregulating these genes increased cell viability and attenuated apoptosis in cells exposed to PM2.5. Conversely, overexpressing TRPV6 exacerbated cell apoptosis caused by PM2.5, while a reactive oxygen species (ROS) inhibitor N-acetyl-l-cysteine (NAC) alleviated PM2.5-induced apoptosis. In conclusion, ATP1A2, MT1M, SLC6A19 and TRPV6 may be contributing to absorption of metals in PM2.5 thereby inducing apoptosis mediated by ROS. Therefore, they hold potential as therapeutic targets for PM2.5-related diseases.

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Recent advances in understanding the mechanisms of PM2.5-mediated neurodegenerative diseases

Cited by 34 publications

References 90 publications

Powdered Green Tea (Matcha) Attenuates the Cognitive Dysfunction via the Regulation of Systemic Inflammation in Chronic PM2.5-Exposed BALB/c Mice

Powdered Green Tea (Matcha) Attenuates the Cognitive Dysfunction via the Regulation of Systemic Inflammation in Chronic PM2.5-Exposed BALB/c Mice

Micro- and Nanosized Substances Cause Different Autophagy-Related Responses

CRISPR/Cas9-Mediated Whole Genomic Wide Knockout Screening Identifies Specific Genes Associated With PM2.5-Induced Mineral Absorption in Liver Toxicity

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